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Chrysin (5, 7-dihydroxyflavone) is a natural flavonoid, known for its antiviral and hepatoprotective activities. However, its anti-HBV activity is unexplored. In the present study, the anti-hepatitis B activity of chrysin was investigated using the in vitro experimental cell culture model, HepG2 cells. In silico studies were performed where chrysin and lamivudine (used here as a positive control) were docked with high mobility group box 1 protein (HMGB1). For the in vitro studies, wild type HBV genome construct (pHBV 1.3X) was transiently transfected in HepG2. In culture supernatant samples, HBV surface antigen (HBsAg) and Hepatitis B e antigen (HBeAg) were measured by enzyme-linked immunosorbent assay (ELISA). Secreted HBV DNA and intracellular covalently closed circular DNA (cccDNA) were measured by SYBR green real-time PCR. The 3D crystal structure of HMGB1 (1AAB) protein was developed and docked with the chrysin and lamivudine. In silico drug-likeness, Absorption, Distribution, Metabolism, Excretion and Toxicity (ADMET) properties of finest ligands were performed by using SwissADME and admetSAR web servers. Data showed that chrysin significantly decreases HBeAg, HBsAg secretion, supernatant HBV DNA and cccDNA, in a dose dependent manner. The docking studies demonstrated HMGB1 as an important target for chrysin as compared to lamivudine. Chrysin revealed high binding affinity and formed a firm kissing complex with HMGB1 (∆G = − 5.7 kcal\u002Fmol), as compared to lamivudine (∆G = − 4.3 kcal\u002Fmol), which might be responsible for its antiviral activity. The outcome of our study establishes chrysin as a new antiviral against HBV infection. However, using chrysin to treat chronic HBV disease needs further endorsement and optimization by in vivo studies in animal models. \n                  \n                    \n                      \n                    \n                  \n                ",{"EN":133},"Potential antiviral activities of chrysin against hepatitis B virus",{"VOID":135},"[\"823433213851577080\"]",{"VOID":137},"Tao Y, et al. Present and future therapies for chronic hepatitis B. Adv Exp Med Biol. 2020;1179:137–86.\nFung J. Prevention of hepatitis B virus recurrence. Hepat Res. 2021;7:33.\nYan H, et al. Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus. Elife. 2012;1:e00049–e00049.\nTu T, Zhang H, Urban S. Hepatitis B virus DNA integration: in vitro models for investigating viral pathogenesis and persistence. Viruses. 2021;13(2):180.\nYe J, Chen J. Interferon and hepatitis B: current and future perspectives. Front Immunol. 2021;12:733364.\nLeowattana W, Leowattana T. Chronic hepatitis B: New potential therapeutic drugs target. World J Virol. 2022;11(1):57–72.\nLee S, et al. Suppression of hepatitis B virus through therapeutic activation of RIG-I and IRF3 signaling in hepatocytes. iScience. 2021;24(1):101969.\nBottecchia M, et al. Monitoring the emergence of HBV resistance mutations by HBV-RNA pyrosequencing. Braz J Infect Dis. 2016;20(2):216–7.\nYuan C, et al. Reactivation of occult hepatitis b virus infection during long-term entecavir antiviral therapy. Front Microbiol. 2022;13:865124.\nNassal M. HBV cccDNA: viral persistence reservoir and key obstacle for a cure of chronic hepatitis B. Gut. 2015;64(12):1972–84.\nSun F, Liu Z, Wang B. Correlation between low-level viremia and hepatitis B-related hepatocellular carcinoma and recurrence: a retrospective study. BMC Cancer. 2021;21(1):1103.\nHuang K, et al. 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Glycyrrhetinic acid alleviates hepatic inflammation injury in viral hepatitis disease via a HMGB1-TLR4 signaling pathway. Int Immunopharmacol. 2020;84:106578–106578.\nNarkhede RR, et al. Recognition of natural products as potential inhibitors of COVID-19 main protease (Mpro): in-silico evidences. Nat Prod Bioprospect. 2020;10(5):297–306.\nZafar F, et al. Physicochemical and pharmacokinetic analysis of anacardic acid derivatives. ACS Omega. 2020;5(11):6021–30.\nSrimai V, et al. Computer-aided design of selective cytochrome P450 inhibitors and docking studies of alkyl resorcinol derivatives. Med Chem Res. 2013;22(11):5314–23.\nMarques SM, et al. Screening of natural compounds as P-glycoprotein inhibitors against multidrug resistance. Biomedicines. 2021;9(4):357.\nJuvonen RO, et al. Substrate selectivity of coumarin derivatives by human CYP1 enzymes: in vitro enzyme kinetics and in silico modeling. ACS Omega. 2021;6(17):11286–96.",{"VOID":139},"10.1186\u002Fs13099-023-00531-6","PUBLICATION","VERIFIED","2024-06-24T23:00:22.417+00:00","Auto Verify","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-023-00531-6",[146,164,179,194,209,233,247,260,283,297,311,327],{"id":147,"sortIndex":21,"researcher":20,"roles":148,"affiliations":150,"properties":159,"displayName":161,"givenName":20,"familyName":20},"c9437458-0570-4627-954d-3653d616e755",[149],"AUTHOR",[151],{"id":152,"sortIndex":21,"affiliation":153,"properties":20},"9893a914-a205-4d0b-842b-1574e88c3d67",{"id":152,"createTime":20,"updateTime":20,"relativeEntities":154,"slug":20,"properties":155,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":158,"statistic":20},[],{"title":156},{"VI":157},"Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi, India",[],{"title":160,"gsAuthor":162},{"VI":161},"Sajad Ahmad Bhat",{"VOID":163},"[\"zyIP89AAAAAJ\"]",{"id":165,"sortIndex":112,"researcher":20,"roles":166,"affiliations":167,"properties":174,"displayName":176,"givenName":20,"familyName":20},"2d975b9f-f2e2-4142-8918-15d64c5a6ad7",[149],[168],{"id":152,"sortIndex":21,"affiliation":169,"properties":20},{"id":152,"createTime":20,"updateTime":20,"relativeEntities":170,"slug":20,"properties":171,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":173,"statistic":20},[],{"title":172},{"VI":157},[],{"title":175,"gsAuthor":177},{"VI":176},"Syed Kazim 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species are common human enteric parasites. Carriage has been linked to Irritable Bowel Syndrome (IBS). Treatment of Blastocystis spp. with antimicrobials is problematic and insensitive diagnostic methods and re-infection complicate assessment of eradication. We investigated whether triple antibiotic therapy comprising diloxanide furoate, trimethoprim\u002Fsulfamethoxazole and secnidazole (TAB) given to diarrhoea-predominant IBS (D-IBS) patients positive for Blastocystis would achieve eradication. In a longitudinal, prospective case study 10 D-IBS Blastocystis-positive patients took 14 days of diloxanide furoate 500 mg thrice daily, trimethoprim\u002Fsulfamethoxazole 160\u002F80 mg twice daily and secnidazole 400 mg thrice daily. Faecal specimens were collected at baseline, day 15 and 4 weeks after completion of TAB. Specimens were analysed using faecal smear, culture and polymerase chain reaction (PCR) of the 16 SSU rRNA. Patients kept a concurrent clinical diary. Six (60%) patients cleared Blastocystis spp. after TAB, including three who had failed previous therapy. Subtypes detected were ST3 (60%), ST4 (40%), ST1 (20%) and ST7, 8 (10%); four patients had mixed ST infections. Serum immunoglobulin A (IgA) levels were low in 40% of patients. Higher rates of Blastocystis clearance were observed in patients symptomatic for less than a year (Mann-Whitney, p?=?0.032, 95% confidence) with no associations found with age, previous antibiotic therapy, faecal parasite load, ST, IgA level or clinical improvement. Clearance of Blastocystis spp. was achieved with TAB in 60% of D-IBS patients, an improvement over conventional monotherapy. Higher clearance rates are needed to facilitate investigation of the relevance of this parasite in clinically heterogenous IBS.",{"EN":424},"Clinical pilot study: efficacy of triple antibiotic therapy in Blastocystis positive irritable bowel syndrome patients",{"VOID":426},"[\"15923707766350798514\"]",{"VOID":428},"Tan KS: New insights on classification, identification, and clinical relevance of Blastocystis spp. Clin Microbiol Rev. 2008, 21 (4): 639-665. 10.1128\u002FCMR.00022-08.\nJimenez-Gonzalez DEM-FW, Reues-Gordillo J, Ramirez-Mirnada M, Arroyo-Escalante S, Romero-Valdovinos M, Stark D, Souza-Saldivar V, Martinez-Hernandez F, Flisser A, Olivo-Diaz A, Maravilla P: Blastocystis infection is associated with irritable bowel syndrome in a Mexican patient population. Parasitol Res. 2012, 110 (3): 1269-1275. 10.1007\u002Fs00436-011-2626-7.\nDogruman-Al F, Simsek Z, Boorom K, Ekici E, Sahin M, Tuncer C, Kustimur S, Altinbas A: Comparison of methods for detection of Blastocystis infection in routinely submitted stool samples, and also in IBS\u002FIBD Patients in Ankara, Turkey. PLoS One. 2010, 5 (11): e15484-10.1371\u002Fjournal.pone.0015484.\nDrossman DA: Introduction. The Rome Foundation and Rome III. Neurogastroenterol Motil. 2007, 19 (10): 783-786. 10.1111\u002Fj.1365-2982.2007.01001.x.\nInadomi JMFM, Bjorkman D: The economic impact of irritable bowel syndrome. Aliment Pharmacol Therapeut. 2003, 18 (7): 671-682. 10.1046\u002Fj.1365-2036.2003.t01-1-01736.x.\nBeatty JKBA, Buret AG: Post-infectious irritable bowel syndrome: Mechanistic insights into chronic disturbances following enteric infection. World J Gastroenterol. 2014, 20 (14): 3976-3985. 10.3748\u002Fwjg.v20.i14.3976.\nCollins S: A role for the gut microbiota in IBS. Nat Rev Gastroenterol Hepatol. 2014, 11 (8): 497-505. 10.1038\u002Fnrgastro.2014.40.\nDuPont H: Review article: evidence for the role of gut microbiota in irritable bowel syndorme and its potential influence on therapeutic targets. Aliment Pharmacol Ther. 2014, 39: 1033-1042. 10.1111\u002Fapt.12728.\nde Salonen A, Vos WM, Palva A: Gastrointestinal microbiota in irritable bowel syndrome:present state and perspectives. Microbiology. 2010, 156: 3205-3215. 10.1099\u002Fmic.0.043257-0.\nMatricon JM, Gelot A, Piche T, Dapoigny M, Muller E, Ardid D: Review article:associations between immune activation, intestinal permeability and the irritable bowel syndrome. Aliment Pharmacol Ther. 2012, 36: 1009-1031. 10.1111\u002Fapt.12080.\nLA Bruewer M, Kucharzik T, Parkos CA, Madara JL, Hopkins AM, Nusrat A: Proinflammatory cytokines disrupt epithelial barrier funciton by apoptosis-independent mechanisms. J Immunol. 2003, 171: 6164-6172. 10.4049\u002Fjimmunol.171.11.6164.\nSteck NMK, Schermann M, Haller D: Bacterial proteases in IBD and IBS. Gut. 2014, 61: 1610-1618. 10.1136\u002Fgutjnl-2011-300775.\nGecse K, Roka R, Ferrier L, Eutamene H, Cartier C, Ait-Belgnaoui A, Rosztoczy A, Izbeki F, Fioramonti J, Wittmann T, Bueno L: Increased faecal serine protease activity in diarrhoeic IBS patients: a colonic luminal factor impairing colonic permeability and sensitivity. Gut. 2008, 57 (5): 591-599. 10.1136\u002Fgut.2007.140210.\nPuthia MK, Lu J, Tan KS: Blastocystis ratti contains cysteine proteases that mediate interleukin-8 response from human intestinal epithelial cells in an NF-kappaB-dependent manner. Eukaryot Cell. 2008, 7 (3): 435-443. 10.1128\u002FEC.00371-07.\nPuthia MK, Sio SWS, Lu J, Tan KSW: Blastocystis ratti Induces contact-independent apoptosis, F-actin rearrangement, and barrier function disruption in IEC-6 cells. Infect Immun. 2006, 74 (7): 4114-4123. 10.1128\u002FIAI.00328-06.\nPuthia MK, Vaithilingam A, Lu J, Tan KS: Degradation of human secretory immunoglobulin A by Blastocystis. Parasitol Res. 2005, 97 (5): 386-389. 10.1007\u002Fs00436-005-1461-0.\nMirza H, Tan KS: Blastocystis exhibits inter- and intra-subtype variation in cysteine protease activity. Parasitol Res. 2009, 104 (2): 355-361. 10.1007\u002Fs00436-008-1203-1.\nWu B, Yin J, Texier C, Roussel M, Tan KS: Blastocystis legumain is localized on the cell surface, and specific inhibition of its activity implicates a pro-survival role for the enzyme. J Biol Chem. 2010, 285 (3): 1790-1798. 10.1074\u002Fjbc.M109.049064.\nYakoob J, Jafri W, Beg MA, Abbas Z, Naz S, Islam M, Khan R: Irritable bowel syndrome: is it associated with genotypes of Blastocystis hominis. Parasitol Res. 2010, 106 (5): 1033-1038. 10.1007\u002Fs00436-010-1761-x.\nStensvold CR: Comparison of Sequencing (Barcode Region) and Sequence-Tagged-Site PCR for Blastocystis Sub-typing. J Clin Microbiol. 2013, 51: 190-194. 10.1128\u002FJCM.02541-12.\nStensvold CR, Smith HV, Nagel R, Olsen KE, Traub RJ: Eradication of Blastocystis carriage with antimicrobials: reality or delusion?. J Clin Gastroenterol. 2009, 44 (2): 85-90. 10.1097\u002FMCG.0b013e3181bb86ba.\nNagel R, Cuttell L, Stensvold CR, Mills PC, Bielefeldt-Ohmann H, Traub RJ: Blastocystis subtypes in symptomatic and asymptomatic family members and pets and response to therapy. Intern Med J. 2012, 42 (11): 1187-1195. 10.1111\u002Fj.1445-5994.2011.02626.x.\nJones DR: A medium for investigating the breakdown of pectin by bacteria. Nature. 1946, 158 (4018): 625-10.1038\u002F158625b0.\nWong KH, Ng GC, Lin RT, Yoshikawa H, Taylor MB, Tan KS: Predominance of subtype 3 among Blastocystis isolates from a major hospital in Singapore. Parasitol Res. 2008, 102 (4): 663-670. 10.1007\u002Fs00436-007-0808-0.\nKumar S, Tamura K, Jakobsen IB, Nei M: MEGA2:Molecular Evolutionary Genetics Analysis software. Bioinformatics. 2001, 17 (12): 1244-1245. 10.1093\u002Fbioinformatics\u002F17.12.1244.\nRoberts T, Ellis J, Harkness J, Marriott D, Starl D: Treatment failure in patients with chronic Blastocystis infection. J Med Microbiol. 2014, 63: 252-257. 10.1099\u002Fjmm.0.065508-0.\nLA Dunn TK, Vanelle P, Juspin T, Crozet MD, Terme T, Upcroft P, Upcroft JA: Development of metronidazole-resistant lines of Blastocystis spp. Parasitol Res. 2012, 111: 441-450. 10.1007\u002Fs00436-012-2860-7.\nMirza H, Teo JDW, Upcroft J, Tan KSW: A rapid, high-throughput viability assay for Blastocystis spp. reveals metronidazole resistance and extensive subtype-dependent variations in drug susceptibilities. Antimicrob Agents Chemother. 2010, 55 (2): 637-648. 10.1128\u002FAAC.00900-10.\nZierdt CH, Swan JC, Hosseini J: In vitro response of Blastocystis hominis to antiprotozoal drugs. J Protozool. 1983, 30 (2): 332-334. 10.1111\u002Fj.1550-7408.1983.tb02925.x.\nVdovenko AA, Williams JE: Blastocystis hominis: neutral red supravital staining and its application to in vitro drug sensitivity testing. Parasitol Res. 2000, 86 (7): 573-581. 10.1007\u002FPL00008533.\nDunn LA, Boreham PF: The in-vitro activity of drugs against Blastocystis hominis. J Antimicrob Chemother. 1991, 27 (4): 507-516. 10.1093\u002Fjac\u002F27.4.507.\nLamp KCFC, Klutman NE, Lacy MK: Pharmacokinetics and Pharmacodynamics of the Nitroimidazole Antimicrobials. Clin Pharmacokinet. 1999, 36 (5): 353-373. 10.2165\u002F00003088-199936050-00004.\nCoyle CMJV, Louis Weiss M, Herbert Tanowitz B: Blastocystis: to treat or not to treat. 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NEJM. 2011, 364: 22-32. 10.1056\u002FNEJMoa1004409.\nAmenta M, Dalle Nogare ER, Colomba C, Prestileo T, Di Lorenzo F, Fundaro S, Colomba A, Ferrieri A: Intestinal protozoa in HIV-infected patients: effect of rifaximin in Cryptosporidium parvum and Blastocystis hominis infections. J Chemother. 1999, 11 (5): 391-395. 10.1179\u002Fjoc.1999.11.5.391.\nGadkariem EA, Belal F, Abounassif MA, El-Obeid HA, Ibrahim KE: Stability studies on diloxanide furoate: effect of pH, temperature, gastric and intestinal fluids. Il Farmaco. 2004, 59: 323-329. 10.1016\u002Fj.farmac.2003.11.015.\nLi LH, Zhang XP, Lv S, Zhang L, Yoshikawa H, Wu Z, Steinmann P, Utzinger J, Tong X, Chen S, Zhou X: Cross-sectional surveys and subtype classification of human Blastocystis isolates from four epidemiological settings in China. Parasitol Res. 2007, 102 (1): 83-90. 10.1007\u002Fs00436-007-0727-0.\nPoirier P, Wawrzyniak I, Albert A, El Alaoui H, Delbac F, Livrelli V: Development and evaluation of a real-time PCR assay for detection and quantification of blastocystis parasites in human stool samples: prospective study of patients with hematological malignancies. J Clin Microbiol. 2011, 49 (3): 975-983. 10.1128\u002FJCM.01392-10.\nTasova Y, Sahin B, Koltas S, Paydas S: Clinical significance and frequency of Blastocystis hominis in Turkish patients with hematological malignancy. Acta Med Okayama. 2000, 54 (3): 133-136.\nOlivo-Diaz A, Romero-Valdovinos M, Gudino-Ramirez A, Reyes-Gordillo J, Jimenez-Gonzalez D, Ramirez-Miranda M, Martinez-Flores W, Martinez-Hernandez F, Flisser A, Maravilla P: Findings related to IL-8 and IL-10 gene polymorphisms in a Mexican patient population with irritable bowel syndrome infected with Blastocystis. Parasitol Res. 2012, 111: 487-491. 10.1007\u002Fs00436-012-2830-0.\nSingh K, Chang C, Gershwin M: IgA deficiency and autoimmunity. Autoimmun Rev. 2014, 13: 163-177. 10.1016\u002Fj.autrev.2013.10.005.\nStoop JW, Zegers B, Sander P, Ballieux R: Serum immunoglobulin levels in healthy children and adults. Clin exp Immunol. 1969, 4: 101-112.\nSuresh K, Venilla GD, Tan TC, Rohela M: In vivo encystation of Blastocystis hominis. Parasitol Res. 2009, 104: 303-307. 10.1007\u002Fs00436-009-1340-1.\nStensvold CR, Arendrup M, Jespersgaard C, Molbak K, Nielsen H: Detecting Blastocystis using parasitologic and DNA-based methods: a comparative study. Diag Microbiol Inf Dis. 2007, 59: 303-307. 10.1016\u002Fj.diagmicrobio.2007.06.003.\nHussain R, Jaferi W, Zuberi A, Baqai R, Abrar N, Ahmed A, Zaman V: Significantly increased IgG2 subclass antibody levels in patients with irritable Bowel Syndrome. Am J Trop Med Hyg. 1997, 56: 301-306.\nAbou Gamra M, Elwakil H, El Deeb H, Khalifa K, Abd Elhafiz H: The potential us of 29 kDa protein as a marker of pathogenicity and diagnosis of symptomatic infections with Blastocystis hominis. Parasitol Res. 2011, 108: 1139-1146. 10.1007\u002Fs00436-010-2156-8.\nGardner T, Hill D: Treatment of giardiasis. Clin Microbiol Rev. 2001, 14: 114-128. 10.1128\u002FCMR.14.1.114-128.2001.",{"VOID":430},"10.1186\u002Fs13099-014-0034-0","2024-05-15T17:52:41.340+00:00","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-014-0034-0",[434,459,481],{"id":435,"sortIndex":21,"researcher":20,"roles":436,"affiliations":437,"properties":454,"displayName":456,"givenName":20,"familyName":20},"11b7deb6-05c2-412a-adbc-4fb539393e3a",[149],[438,446],{"id":439,"sortIndex":21,"affiliation":440,"properties":20},"0c69d955-50bc-4155-872d-1c0e426fa658",{"id":439,"createTime":20,"updateTime":20,"relativeEntities":441,"slug":20,"properties":442,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":445,"statistic":20},[],{"title":443},{"VI":444},"School of Veterinary Science, The University of Queensland, Gatton, 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an effector mediator, targets Notch-1 and regulates the innate and adaptive immune systems response. Recently, we reported that Notch-1 signaling plays a key role in macrophage polarization and response during infection. We employed Mycobacterium avium paratuberculosis (MAP) infection in Crohn’s disease (CD) as a model to demonstrate the role of Notch-1\u002FIL-6 signaling on MCL-1 based apoptosis and intracellular MAP infection and persistence. This study was designed to investigate the impact of polymorphisms in miR146a on the immune response and infection in our MAP-CD model. We determined the incidence of miR-146a rs2910164 G > C in 42 blood samples from clinical CD patients and controls. We also measured the effect of rs2910164 on expression of Notch-1 and IL-6, and plasma IL-6 protein levels in our study group. Finally, we analyzed the blood samples for MAP DNA and studied any correlation with miR-146a polymorphism. Samples were analyzed for statistical significance using unpaired tow-tailed t-test, unpaired two-tailed z-score and odds ratio. P \u003C 0.05 considered significant. MiR-146a rs2910164 GC was detected at a higher incidence in CD (52.6%) compared to healthy controls (21.7%) rs2910164 GC Heterozygous polymorphism upregulated Notch-1 and IL-6, by 0.9 and 1.7-fold, respectively. As expected, MAP infection was detected more in CD samples (63%) compared to healthy controls (9%). Surprisingly, MAP infection was detected at a higher rate in samples with rs2910164 GC (67%) compared to samples with normal genotype (33%). The data clearly associates miR-146a rs2910164 GC with an overactive immune response and increases the risk to acquire infection. The study is even more relevant now in our efforts to understand susceptibility to SARS-CoV-2 infection and the development of COVID-19. This study suggests that genetic variations among COVID-19 patients may predict who is at a higher risk of acquiring infection, developing exacerbating symptoms, and possibly death. A high scale study with more clinical samples from different disease groups is planned.",{"EN":577},"MiR-146a rs2910164 G > C polymorphism modulates Notch-1\u002FIL-6 signaling during infection: a possible risk factor for Crohn’s disease",{"VOID":579},"[\"5774280118943311348\"]",{"VOID":581},"10.1186\u002Fs13099-020-00387-0","2024-05-03T12:30:45.004+00:00","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-020-00387-0",[585,602],{"id":586,"sortIndex":21,"researcher":20,"roles":587,"affiliations":588,"properties":597,"displayName":599,"givenName":20,"familyName":20},"df1faca7-2cc8-4b7e-a08b-61fd095fde41",[149],[589],{"id":590,"sortIndex":21,"affiliation":591,"properties":20},"1cd47eb1-f071-479f-878e-0243672029ee",{"id":590,"createTime":20,"updateTime":20,"relativeEntities":592,"slug":20,"properties":593,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":596,"statistic":20},[],{"title":594},{"VI":595},"Division of Molecular Microbiology, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, USA",[],{"title":598,"gsAuthor":600},{"VI":599},"Esra’a Keewan",{"VOID":601},"[\"2UNIqbAAAAAJ\"]",{"id":603,"sortIndex":112,"researcher":20,"roles":604,"affiliations":605,"properties":612,"displayName":614,"givenName":20,"familyName":20},"2d381bce-b116-49a3-92b3-a9639ce2ef80",[149],[606],{"id":590,"sortIndex":21,"affiliation":607,"properties":20},{"id":590,"createTime":20,"updateTime":20,"relativeEntities":608,"slug":20,"properties":609,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":611,"statistic":20},[],{"title":610},{"VI":595},[],{"title":613,"gsAuthor":615},{"VI":614},"Saleh A. 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MicroRNA-146a protects against LPS-induced organ damage by inhibiting Notch1 in macrophage. Int Immunopharmacol. 2018 Oct;1:63:220–6.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1567576918303692",{"doi":728},"10.1016\u002Fj.intimp.2018.07.040",{"id":694,"text":730,"url":696,"identifiers":731},"Rusca N, Monticelli S. MiR-146a in immunity and disease. Mol Biol Int. 2011;2011:437301.",{"doi":698},{"id":694,"text":733,"url":696,"identifiers":734},"Jazdzewski K, Murray EL, Franssila K, Jarzab B, Schoenberg DR, de la Chapelle A. Common SNP in pre-miR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma. Proc Natl Acad Sci. 2008;105(20):7269–74.",{"doi":698},{"id":694,"text":736,"url":696,"identifiers":737},"Ahmadi K, Soleimani A, Motlagh SS, Ahmadi SB, Almasian M, Kiani AA. 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Front Cell Infect Microbiol. 2018;8:11.",{"doi":698},{"id":757,"text":758,"url":759,"identifiers":760},"a5fa0d28-5879-40fd-a883-305643adab8e","Naser SA, Thanigachalam S, Dow CT, Collins MT. Exploring the role of Mycobacterium avium subspecies paratuberculosis in the pathogenesis of type 1 diabetes mellitus: a pilot study. Gut Pathog. 2013;5(1):14.","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002F1757-4749-5-14",{"doi":761},"10.1186\u002F1757-4749-5-14",{"id":763,"text":764,"url":765,"identifiers":766},"130e2b8e-2afc-4422-8cea-066dad46cd4f","Naser SA, Ghobrial G, Romero C, Valentine JF. Culture of Mycobacterium avium subspecies paratuberculosis from the blood of patients with Crohn’s disease. Lancet. 2004;18(9439):1039–44.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS014067360417058X",{"doi":767},"10.1016\u002Fs0140-6736(04)17058-x",{"id":694,"text":769,"url":696,"identifiers":770},"Sharp RC, Beg SA, Naser SA. Role of PTPN2\u002F22 polymorphisms in pathophysiology of Crohn’s disease. World J Gastroenterol. 2018;24(6):657.",{"doi":698},{"id":772,"text":773,"url":774,"identifiers":775},"ecc894fe-5d7c-467b-9906-de6cfc4d788e","Alcedo KP, Thanigachalam S, Naser SA. RHB-104 triple antibiotics combination in culture is bactericidal and should be effective for treatment of Crohn’s disease associated with Mycobacterium paratuberculosis. Gut Pathog. 2016;8(1):32.","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-016-0115-3",{"doi":776},"10.1186\u002Fs13099-016-0115-3",{"id":20,"text":778,"url":20,"identifiers":779},"Roda G, Ng SC, Kotze PG, Argollo M, Panaccione R, Spinelli A, Kaser A, Peyrin-Biroulet L, Danese S. Crohn’s disease. Nat Rev Dis Primers. 2020;2(1):1–9.",{},{"id":694,"text":781,"url":696,"identifiers":782},"Alatab S, Sepanlou SG, Ikuta K, Vahedi H, Bisignano C, Safiri S, Sadeghi A, Nixon MR, Abdoli A, Abolhassani H, Alipour V. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol. 2020;5(1):17–30.",{"doi":698},{"id":694,"text":784,"url":696,"identifiers":785},"Rohr M, Narasimhulu CA, Sharma D, Doomra M, Riad A, Naser S, Parthasarathy S. Inflammatory diseases of the gut. J Med Food. 2018;21(2):113–26.",{"doi":698},{"id":694,"text":787,"url":696,"identifiers":788},"Norton BA, Thomas R, Lomax KG, Dudley-Brown S. Patient perspectives on the impact of Crohn’s disease: results from group interviews. Patient Prefer Adher. 2012;6:509.",{"doi":698},{"id":694,"text":790,"url":696,"identifiers":791},"Chamberlin W, Graham DY, Hulten K, El-Zimaity HM, Schwartz MR, Naser S, Shafran I, El-Zaatari FA. Mycobacterium avium subsp. paratuberculosis as one cause of Crohn’s disease. Aliment Pharmacol Ther. 2001;15(3):337–46.",{"doi":698},{"id":694,"text":793,"url":696,"identifiers":794},"Frade-Proud’Hon-Clerc S, Smol T, Frenois F, Sand O, Vaillant E, Dhennin V, Bonnefond A, Froguel P, Fumery M, Guillon-Dellac N, Gower-Rousseau C. A novel rare missense variation of the NOD2 gene: evidences of implication in Crohn’s disease. Int J Mol Sci. 2019;20(4):835.",{"doi":698},{"id":694,"text":796,"url":696,"identifiers":797},"He Y, Sun X, Huang C, Long XR, Lin X, Zhang L, Lv XW, Li J. MiR-146a regulates IL-6 production in lipopolysaccharide-induced RAW264 7 macrophage cells by inhibiting Notch1. Inflammation. 2014;37(1):71–82.",{"doi":698},{"id":694,"text":799,"url":696,"identifiers":800},"Zhang M, Sun K, Wu Y, Yang Y, Tso P, Wu Z. Interactions between intestinal microbiota and host immune response in inflammatory bowel disease. Front Immunol. 2017;8:942.",{"doi":698},{"id":694,"text":802,"url":696,"identifiers":803},"Mahida YR, Kurlac L, Gallagher A, Hawkey CJ. High circulating concentrations of interleukin-6 in active Crohn’s disease but not ulcerative colitis. Gut. 1991;32(12):1531–4.",{"doi":698},{"id":805,"text":806,"url":807,"identifiers":808},"500c07f5-4c63-4ace-8d72-fdc43835ef24","Singh PP, Goyal A. Interleukin-6: a potent biomarker of mycobacterial infection. Springerplus. 2013 Dec;1(1):686.","https:\u002F\u002Fspringerplus.springeropen.com\u002Farticles\u002F10.1186\u002F2193-1801-2-686",{"doi":809},"10.1186\u002F2193-1801-2-686",{"id":694,"text":811,"url":696,"identifiers":812},"Ulhaq ZS, Soraya GV. Interleukin-6 as a potential biomarker of COVID-19 progression. Méd Mal Infect. 2020;50(4):382–3.",{"doi":698},{"id":694,"text":814,"url":696,"identifiers":815},"Yoshida Y, Tanaka T. Interleukin 6 and rheumatoid arthritis. BioMed Res Int. 2014;2014:698313.",{"doi":698},{"id":694,"text":817,"url":696,"identifiers":818},"Magro G. SARS-CoV-2 and COVID-19: is interleukin-6 (IL-6) the’culprit lesion’of ARDS onset? What is there besides Tocilizumab? SGP130Fc. Cytokine. 2020;14:100029.",{"doi":698},{"id":694,"text":820,"url":696,"identifiers":821},"Michot JM, Albiges L, Chaput N, Saada V, Pommeret F, Griscelli F, Balleyguier C, Besse B, Marabelle A, Netzer F, Merad M. Tocilizumab, an anti-IL-6 receptor antibody, to treat COVID-19-related respiratory failure: a case report. Ann Oncol. 2020;31(7):961–4.",{"doi":698},{"id":823,"createTime":824,"updateTime":825,"relativeEntities":826,"slug":827,"properties":828,"entityType":140,"verifyStatus":141,"verifyTime":839,"verifyNote":143,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":840,"fullTextUrl":20,"authors":841,"publicationType":341,"publisherRelationship":991,"citationCount":20,"citationInfo":20,"publishDate":1053,"publishYear":407,"citationAnalyzeStatus":1054,"lastCitationAnalyze":825,"indexDatabases":1055,"openAccess":20,"references":20,"isForceReanalyzing":413},"297ef958-13f7-4cb9-80cd-a6d711efacf0","2024-02-14T13:04:36.744+00:00","2026-03-05T18:40:51.893+00:00",[],"A-multi-omics-study-to-investigate-the-progression-of-the-Correa-pathway-in-gastric-mucosa-in-the-context-of-cirrhosis",{"abstract":829,"title":831,"gsPaper":833,"references":835,"doi":837},{"EN":830},"Patients with liver cirrhosis (LC) are prone to gastric mucosa damage. We investigated the alterations of gastric mucosa in LC patients and their possible mechanisms through multi-omics. We observed significant gastric mucosa microbial dysbiosis in LC subjects. Gastric mucosal microbiomes of LC patients contained a higher relative abundance of Streptococcus, Neisseria, Prevotella, Veillonella, and Porphyromonas, as well as a decreased abundance in Helicobacter and Achromobacter, than control subjects. The LC patients had higher levels of bile acids (BAs) and long-chain acylcarnitines (long-chain ACs) in serum. The gastric mucosal microbiomes were associated with serum levels of BAs and long-chain ACs. Transcriptome analyses of gastric mucosa revealed an upregulation of endothelial cell specific molecule 1, serpin family E member 1, mucin 2, caudal type homeobox 2, retinol binding protein 2, and defensin alpha 5 in LC group. Besides, the bile secretion signaling pathway was significantly upregulated in the LC group. The alterations in the gastric mucosal microbiome and transcriptome of LC patients were identified. The impaired energy metabolism in gastric mucosal cells and bile acids might aggravate the inflammation of gastric mucosa and even exacerbate the Correa’s cascade process. The gastric mucosal cells might reduce bile acid toxicity by bile acid efflux and detoxification. Trial registration: ChiCTR2100051070.",{"EN":832},"A multi-omics study to investigate the progression of the Correa pathway in gastric mucosa in the context of cirrhosis",{"VOID":834},"[]",{"VOID":836},"Sepanlou SG, Safiri S, Bisignano C, Ikuta KS, Merat S, Saberifiroozi M, Poustchi H, Tsoi D, Colombara DV, Abdoli A, Adedoyin RA. The global, regional, and national burden of cirrhosis by cause in 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol. 2020;5:245–66.\nAlbillos A, de Gottardi A, Rescigno M. 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Ann Transl Med. 2014;2:7.",{"VOID":838},"10.1186\u002Fs13099-023-00571-y","2024-05-11T09:22:57.350+00:00","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-023-00571-y",[842,857,870,885,900,913,926,939,952,965,978],{"id":843,"sortIndex":21,"researcher":20,"roles":844,"affiliations":845,"properties":854,"displayName":856,"givenName":20,"familyName":20},"f68bdf54-6527-413d-a0d8-7d8f20a5edfe",[149],[846],{"id":847,"sortIndex":21,"affiliation":848,"properties":20},"ad69a5c2-d6dc-4531-808d-cc0fae926c74",{"id":847,"createTime":20,"updateTime":20,"relativeEntities":849,"slug":20,"properties":850,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":853,"statistic":20},[],{"title":851},{"VI":852},"Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, China",[],{"title":855},{"VI":856},"Ruiguang 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emergence of the novel GII.17 Kawasaki 2014 norovirus variant raising the interest of the public, has replaced GII.4 as the predominant cause of noroviruses outbreaks in East Asia during 2014–2015. Antigenic variation of the capsid protein is considered as one of the key mechanisms of norovirus evolution. In this study, we screened a panel of GII.17 mutants. First, we produced norovirus P proteins using cell-free protein synthesis (CFPS) system, comparing the results to pure proteins expressed in a cell-based system. Next, we determined the binding capability of specific monoclonal antibody (mAb) 2D11 using a unique set of wild-type GII.17 strains. Results of the EIA involving a panel of mutant cell-free proteins indicated that Q298 was the key residue within loop 1. These data highlighted the essential residues in the linear antibody binding characteristics of novel GII.17. Furthermore, it supported the CFPS as a promising tool for rapidly screening mutants via the scalable expression of norovirus P proteins.",{"EN":1066},"Rapid screening for antigenic characterization of GII.17 norovirus strains with variations in capsid gene",{"VOID":834},{"VOID":1069},"Liao Y, Hong X, Wu A, Jiang Y, Liang Y, Gao J, et al. Global prevalence of norovirus in cases of acute gastroenteritis from 1997 to 2021: an updated systematic review and meta-analysis. Microb Pathog. 2021;161: 105259.\nPayne DC, Vinje J, Szilagyi PG, Edwards KM, Staat MA, Weinberg GA, et al. Norovirus and medically attended gastroenteritis in U.S. Children. N Engl J Med. 2013;368:1121–30.\nShah MP, Hall AJ. Norovirus illnesses in children and adolescents. Infect Dis Clin North Am. 2018;32:103–18.\nBartsch SM, Lopman BA, Ozawa S, Hall AJ, Lee BY. Global economic burden of norovirus gastroenteritis. PLoS ONE. 2016;11: e0151219.\nTeunis PFM, Moe CL, Liu P, Miller SE, Lindesmith L, Baric RS, et al. Norwalk virus: how infectious is it? J Med Virol. 2008;80:1468–76.\nCates JE, Vinjé J, Parashar U, Hall AJ. Recent advances in human norovirus research and implications for candidate vaccines. Expert Rev Vaccines. 2020;19:539–48.\nFord-Siltz LA, Tohma K, Parra GI. Understanding the relationship between norovirus diversity and immunity. Gut microbes. 2021;13:1–13.\nChan MCW, Lee N, Hung T-N, Kwok K, Cheung K, Tin EKY, et al. Rapid emergence and predominance of a broadly recognizing and fast-evolving norovirus GII.17 variant in late 2014. Nat Commun. 2015;6:10061.\nZheng DP, Widdowson MA, Glass RI, Vinje J. Molecular epidemiology of genogroup II-genotype 4 noroviruses in the United States between 1994 and 2006. J Clin Microbiol. 2010;48:168–77.\nde Graaf M, van Beek J, Vennema H, Podkolzin AT, Hewitt J, Bucardo F, et al. Emergence of a novel GII.17 norovirus—End of the GII.4 era? Euro Surveill. 2015;20:21178.\nParra GI, Squires RB, Karangwa CK, Johnson JA, Lepore CJ, Sosnovtsev SV, et al. Static and evolving norovirus genotypes: implications for epidemiology and immunity. Plos Patho. 2017;13: e1006136.\nSingh BK, Koromyslova A, Hefele L, Gurth C, Hansman GS. Structural evolution of the emerging 2014–2015 GII.17 noroviruses. J Virol. 2015;90:2710–5.\nJin M, Zhou YK, Xie HP, Fu JG, He YQ, Zhang S, et al. Characterization of the new GII.17 norovirus variant that emerged recently as the predominant strain in China. J Gen Virol. 2016;97:2620–32.\nQian Y, Song M, Jiang X, Xia M, Meller J, Tan M, et al. Structural Adaptations of Norovirus GII.17\u002F13\u002F21 lineage through two distinct evolutionary paths. J Virol. 2019;93:e01655-01618.\nHardy ME. Norovirus protein structure and function. FEMS Microbiol Lett. 2005;253:1–8.\nLiu W-Q, Zhang L, Chen M, Li J. Cell-free protein synthesis: recent advances in bacterial extract sources and expanded applications. Biochem Eng J. 2019;141:182–9.\nEndo Y, Sawasaki T. Cell-free expression systems for eukaryotic protein production. Curr Opin Biotech. 2006;17:373–80.\nJackson K, Khnouf R, Fan ZH. Cell-free protein synthesis in microfluidic 96-well plates. Methods in Mol Biol (Clifton, NJ). 2014;1118:157–68.\nFu L, Niu B, Zhu Z, Wu S, Li W. CD-HIT: accelerated for clustering the next-generation sequencing data. Bioinformatics. 2012;28:3150–2.\nKatoh K, Standley DM. MAFFT multiple sequence alignment software version 7: improvements in performance and usability. Mol Biol Evol. 2013;30:772–80.\nDarriba D, Taboada GL, Doallo R, Posada D. jModelTest 2: more models, new heuristics and parallel computing. Nat methods. 2012;9:772.\nGuindon S, Dufayard JF, Lefort V, Anisimova M, Hordijk W, Gascuel O. New algorithms and methods to estimate maximum-likelihood phylogenies assessing the performance of PhyML 3.0. Syst Biol. 2010;59:307–21.\nSuchard MA, Lemey P, Baele G, Ayres DL, Drummond AJ, Rambaut A. Bayesian phylogenetic and phylodynamic data integration using BEAST 1.10. Virus Evolution. 2018;4(1):vey016.\nXue L, Dong R, Wu Q, Li Y, Cai W, Kou X, et al. Molecular epidemiology of noroviruses associated with sporadic gastroenteritis in Guangzhou, China, 2013–2015. Arch Virol. 2016;161:1377–84.\nXue L, Cai W, Wu Q, Zhang J, Guo W. Direct sequencing and analysis of the genomes of newly emerging GII17 norovirus strains in South China. J Appl Microbiol. 2016;120:1130–5.\nArnold K, Bordoli L, Kopp J, Schwede T. The SWISS-MODEL workspace: a web-based environment for protein structure homology modelling. Bioinformatics. 2006;22:195–201.\nLindesmith LC, Debbink K, Swanstrom J, Vinjé J, Costantini V, Baric RS, et al. Monoclonal antibody-based antigenic mapping of norovirus GII.4-2002. J Virol. 2012;86:873–83.\nLindesmith LC, Brewer-Jensen PD, Mallory ML, Yount B, Collins MH, Debbink K, et al. Human Norovirus Epitope D plasticity allows escape from antibody immunity without loss of capacity for binding cellular ligands. J Virol. 2019;93:e01813-01818.\nSheng J, Lei S, Yuan L, Feng X. Cell-free protein synthesis of norovirus virus-like particles. RSC Adv. 2017;7:28837–40.\nLindesmith LC, Kocher JF, Donaldson EF, Debbink K, Mallory ML, Swann EW, et al. Emergence of novel human norovirus GII.17 strains correlates with changes in blockade antibody epitopes. J Infect Dis. 2017;216:1227–34.\nTohma K, Lepore CJ, Ford-Siltz LA, Parra GI. Evolutionary dynamics of non-GII genotype 4 (GII.4) noroviruses reveal limited and independent diversification of variants. J Gen Virol. 2018;99:1027–35.\nChen H, Qian F, Xu J, Chan M, Shen Z, Zai S, et al. A novel norovirus GII.17 lineage contributed to adult gastroenteritis in Shanghai, China, during the winter of 2014–2015. Emerg Microbes Infect. 2015;4:e67.\nXue L, Wu Q, Cai W, Zhang J, Guo W. Molecular characterization of new emerging GII.17 norovirus strains from South China. Infect Genet Evol. 2016;40:1–7.\nYi Y, Wang X, Wang S, Xiong P, Liu Q, Zhang C, et al. Identification of a blockade epitope of human norovirus GII.17. Emerg Microbes Infect. 2021;10:954–63.\nDebbink K, Donaldson EF, Lindesmith LC, Baric RS. Genetic mapping of a highly variable norovirus GII.4 blockade epitope: potential role in escape from human herd immunity. J Virol. 2012;86:1214–26.\nLindesmith LC, Costantini V, Swanstrom J, Debbink K, Donaldson EF, Vinjé J, et al. Emergence of a norovirus GII.4 strain correlates with changes in evolving blockade epitopes. J Virol. 2013;87:2803–13.\nAllen DJ, Gray JJ, Gallimore CI, Xerry J, Iturriza-Gómara M. Analysis of amino acid variation in the P2 domain of the GII-4 norovirus VP1 protein reveals putative variant-specific epitopes. PLoS ONE. 2008;3: e1485.\nLindesmith LC, Costantini V, Swanstrom J, Debbink K, Donaldson EF, Vinje J, et al. Emergence of a norovirus GII.4 strain correlates with changes in evolving blockade epitopes. J Virol. 2013;87:2803–13.\nDebbink K, Lindesmith LC, Donaldson EF, Costantini V, Beltramello M, Corti D, et al. Emergence of new pandemic GII.4 Sydney norovirus strain correlates with escape from herd immunity. J Infect Dis. 2013;208:1877–87.\nLindesmith LC, Donaldson EF, Baric RS. Norovirus GII.4 strain antigenic variation. J Virol. 2011;85:231–42.\nXue L, Cai W, Gao J, Zhang L, Dong R, Li Y, et al. The resurgence of the norovirus GII.4 variant associated with sporadic gastroenteritis in the post-GII.7 period in South China, 2015 to 2017. BMC Infect Dis. 2019;19:696.\nFiege B, Leuthold M, Parra F, Dalton KP, Meloncelli PJ, Lowary TL, et al. Epitope mapping of histo blood group antigens bound to norovirus VLPs using STD NMR experiments reveals fine details of molecular recognition. 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Wu",{"url":1073,"publisher":1273,"properties":1330},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1274,"slug":10,"properties":1275,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1278,"manageAffiliations":1299,"indexDatabases":1310,"url":20,"thumbnailPath":20,"statistic":1325,"gsStatistic":20,"type":118,"analyzePriority":20},[],{"issn":1276,"title":1277},{"VOID":13},{"EN":15},[1279,1283,1287,1291,1295],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1280,"label":1281,"description":1282,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1284,"label":1285,"description":1286,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":1288,"label":1289,"description":1290,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":1292,"label":1293,"description":1294,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1296,"label":1297,"description":1298,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":51},{},[1300,1305],{"id":55,"createTime":20,"updateTime":20,"relativeEntities":1301,"slug":20,"properties":1302,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1304,"statistic":20},[],{"title":1303},{"EN":59},[],{"id":62,"createTime":20,"updateTime":20,"relativeEntities":1306,"slug":20,"properties":1307,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1309,"statistic":20},[],{"title":1308},{"EN":66},[],[1311,1318],{"id":70,"indexDatabase":1312,"url":83,"indexYears":20,"academicFieldIds":1317,"indexDatabaseRanking":20},{"id":72,"createTime":20,"updateTime":20,"relativeEntities":1313,"label":1314,"description":1315,"key":79,"publicationTags":1316,"standard":20},[],{"EN":75,"VI":75},{"EN":77,"VI":78},[81,82],[85,86],{"id":88,"indexDatabase":1319,"url":99,"indexYears":100,"academicFieldIds":1324,"indexDatabaseRanking":107},{"id":90,"createTime":20,"updateTime":20,"relativeEntities":1320,"label":1321,"description":1322,"key":96,"publicationTags":1323,"standard":20},[],{"EN":93,"VI":93},{"EN":93,"VI":95},[98],[102,103,104,105,106],{"impactFactor":21,"impactFactorByYear":1326,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":110,"totalPublicationByYear":1327,"totalCitation":21,"totalCitationByYear":1328,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":1329,"hindexLast5Year":21,"hindex":21},{},{"2011":112,"2013":112,"2014":112,"2016":112,"2018":112,"2019":112,"2020":112,"2021":113,"2023":114,"2024":115},{},{},{"pages":1331,"volume":1332},{"VOID":1051},{"VOID":1333},"14","2022-07-25",2022,"2026-02-12T00:39:46.143+00:00",[107,81],{"id":1339,"createTime":1340,"updateTime":1341,"relativeEntities":1342,"slug":1343,"properties":1344,"entityType":140,"verifyStatus":141,"verifyTime":1354,"verifyNote":143,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1355,"fullTextUrl":20,"authors":1356,"publicationType":341,"publisherRelationship":1385,"citationCount":20,"citationInfo":20,"publishDate":1448,"publishYear":1449,"citationAnalyzeStatus":1054,"lastCitationAnalyze":1450,"indexDatabases":1451,"openAccess":20,"references":20,"isForceReanalyzing":413},"de4f2e82-89bc-43dc-80b6-8fb3827bacd8","2024-02-14T07:00:05.606+00:00","2026-01-11T23:17:53.912+00:00",[],"Characteristics-of-patients-infected-with-Clostridioides-difficile-at-a-Saudi-Tertiary-Academic-Medical-Center-and-assessment-of-antibiotic-duration",{"abstract":1345,"title":1347,"gsPaper":1349,"references":1350,"doi":1352},{"EN":1346},"Clostridioides difficile infection (CDI) is a common hospital-associated diarrhea. Several antibiotics commonly associate with CDI; however, limited data are available on the duration of exposure prior to CDI. Moreover, studies on the characteristics of CDI patients in Saudi Arabia are limited. Therefore, this study aimed to characterize CDI patients identified over 10 years and assess antibiotic days of therapy (DOT) prior to CDI. This was a retrospective descriptive analysis of CDI patients at a Saudi tertiary academic medical center between December 2007 and January 2018. Patients characteristics, prior exposure to known CDI risk factors, and DOT of antibiotics prior to CDI incidence were assessed. A total of 159 patients were included. Median age was 62 years. Most cases were hospital-acquired (71.1%), non-severe (44.7%), and admitted to medical wards (81.1%). Prior exposure to antibiotics and acid suppression therapy were reported with the majority (76.1 and 75.5%, respectively). The most frequently prescribed antibiotics were piperacillin\u002Ftazobactam, ceftriaxone, meropenem, and ciprofloxacin with median DOTs prior to CDI incidence of 14 days for the β-lactams and 26 days for ciprofloxacin. The distribution of DOT was significantly different for piperacillin\u002Ftazobactam in different units (P = 0.003) where its median DOT was the shortest in medical wards (11 days), and for ciprofloxacin among different severity groups (P = 0.013), where its median DOT was the shortest in severe CDI patients (11 days). Most patients in this study had hospital-acquired non-severe CDI and were largely exposed to antibiotics and acid suppression therapy. Therefore, such therapies should be revised for necessity.",{"EN":1348},"Characteristics of patients infected with Clostridioides difficile at a Saudi Tertiary Academic Medical Center and assessment of antibiotic duration",{"VOID":834},{"VOID":1351},"McDonald LC, Gerding DN, Johnson S, Bakken JS, Carroll KC, Coffin SE, et al. Clinical practice guidelines for Clostridium difficile infection in adults and children: 2017 update by the infectious diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA). Clin Infect Dis. 2018;66(7):987–94. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fcid\u002Fciy149.\nThabit AK, Housman ST, Burnham CD, Nicolau DP. Association of healthcare exposure with acquisition of different Clostridium difficile strain types in patients with recurrent infection or colonization after clinical resolution of initial infection. J Hosp Infect. 2016;92(2):167–72. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhin.2015.11.009.\nCzepiel J, Drozdz M, Pituch H, Kuijper EJ, Perucki W, Mielimonka A, et al. Clostridium difficile infection: review. Eur J Clin Microbiol Infect Dis. 2019;38(7):1211–21. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10096-019-03539-6.\nThabit AK, Varugehese CA, Levine AR. Antibiotic use and duration in association with Clostridioides difficile infection in a tertiary academic medical center: a retrospective case-control study. Anaerobe. 2019;59:126–30. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.anaerobe.2019.06.016.\nLeffler DA, Lamont JT. Clostridium difficile infection. N Engl J Med. 2015;372(16):1539–48. https:\u002F\u002Fdoi.org\u002F10.1056\u002FNEJMra1403772.\nHensgens MP, Goorhuis A, Dekkers OM, Kuijper EJ. Time interval of increased risk for Clostridium difficile infection after exposure to antibiotics. J Antimicrob Chemother. 2012;67(3):742–8. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fjac\u002Fdkr508.\nJohnson S, Samore MH, Farrow KA, Killgore GE, Tenover FC, Lyras D, et al. Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals. N Engl J Med. 1999;341(22):1645–51. https:\u002F\u002Fdoi.org\u002F10.1056\u002Fnejm199911253412203.\nAl-Tawfiq JA, Abed MS. Clostridium difficile-associated disease among patients in Dhahran, Saudi Arabia. Travel medicine and infectious disease. 2010;8(6):373–6. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.tmaid.2010.10.003.\nAl-Tawfiq JA, Rabaan AA, Bazzi AM, Raza S, Noureen M. Clostridioides (Clostridium) difficile-associated disease: epidemiology among patients in a general hospital in Saudi Arabia. Am J Infect Control. 2020. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ajic.2020.01.011.\nAlzouby S, Baig K, Alrabiah F, Shibl A, Al-Nakhli D, Senok AC. Clostridioides difficile infection: Incidence and risk factors in a tertiary care facility in Riyadh. Saudi Arabia J Infect Public Health. 2020;13(7):1012–7. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jiph.2019.10.014.\nMalekzadegan Y, Halaji M, Hasannejad-Bibalan M, Jalalifar S, Fathi J, Ebrahim-Saraie HS. Burden of Clostridium (Clostridioides) difficile infection among patients in Western Asia: a systematic review and meta-analysis. Iran J Public Health. 2019;48(9):1589–99.\nAl Assaad R, Dakessian A, Bachir R, Bizri AR, El Sayed M. Significance of Clostridium difficile in community-acquired diarrhea in a tertiary care center in Lebanon. Sci Rep. 2020;10(1):5678. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41598-020-62418-9.\nKaraoui WR, Rustam LBO, Bou Daher H, Rimmani HH, Rasheed SS, Matar GM, et al. Incidence, outcome, and risk factors for recurrence of nosocomial Clostridioides difficile infection in adults: a prospective cohort study. J Infect Public Health. 2020;13(4):485–90. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jiph.2019.11.005.\nAzimirad M, Krutova M, Yadegar A, Shahrokh S, Olfatifar M, Aghdaei HA, et al. Clostridioides difficile ribotypes 001 and 126 were predominant in Tehran healthcare settings from 2004 to 2018: a 14-year-long cross-sectional study. Emerg Microbes Infect. 2020;9(1):1432–43. https:\u002F\u002Fdoi.org\u002F10.1080\u002F22221751.2020.1780949.\nJamal WY, Rotimi VO. Surveillance of antibiotic resistance among hospital- and community-acquired toxigenic Clostridium difficile Isolates over 5-year period in Kuwait. PLoS ONE. 2016;11(8):e0161411. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0161411.\nNational Healthcare Safety Network. Multidrug-Resistant Organism and Clostridioides difficile Infection (MDRO\u002FCDI) Module. Centers for Disease Control and Prevention, Atlanta, GA. 2021. https:\u002F\u002Fwww.cdc.gov\u002Fnhsn\u002Fpdfs\u002Fpscmanual\u002F12pscmdro_cdadcurrent.pdf.\nBiosynex Group. IMMUNOQUICK®: Clostridium difficile GDH and Tox A\u002FB product catalog. Strasbourg Cedex, France. 2015.\nCenters for Disease Control and Prevention. Antimicrobial Use and Resistance (AUR) Module. Atlanta, GA. 2020.\nHung YP, Lin HJ, Wu TC, Liu HC, Lee JC, Lee CI, et al. Risk factors of fecal toxigenic or non-toxigenic Clostridium difficile colonization: impact of Toll-like receptor polymorphisms and prior antibiotic exposure. PLoS ONE. 2013;8(7):e69577. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0069577.\nMarciniak C, Chen D, Stein AC, Semik PE. Prevalence of Clostridium difficile colonization at admission to rehabilitation. Arch Phys Med Rehabil. 2006;87(8):1086–90. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.apmr.2006.03.020.\nAljafel NA, Al-Shaikhy HH, Alnahdi MA, Thabit AK. Incidence of Clostridioides difficile infection at a Saudi Tertiary Academic Medical Center and compliance with IDSA\u002FSHEA, ACG, and ESCMID guidelines for treatment over a 10-year period. J Infect Public Health. 2020. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jiph.2020.03.007.\nOfori E, Ramai D, Dhawan M, Mustafa F, Gasperino J, Reddy M. Community-acquired Clostridium difficile: epidemiology, ribotype, risk factors, hospital and intensive care unit outcomes, and current and emerging therapies. J Hosp Infect. 2018;99(4):436–42. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhin.2018.01.015.\nChitnis AS, Holzbauer SM, Belflower RM, Winston LG, Bamberg WM, Lyons C, et al. Epidemiology of community-associated Clostridium difficile infection, 2009 through 2011. JAMA internal medicine. 2013;173(14):1359–67. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjamainternmed.2013.7056.\nDial S, Delaney JA, Barkun AN, Suissa S. Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated disease. JAMA. 2005;294(23):2989–95. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjama.294.23.2989.\nBlot E, Escande MC, Besson D, Barbut F, Granpeix C, Asselain B, et al. Outbreak of Clostridium difficile-related diarrhoea in an adult oncology unit: risk factors and microbiological characteristics. J Hosp Infect. 2003;53(3):187–92.\nAnanthakrishnan AN, Issa M, Binion DG. Clostridium difficile and inflammatory bowel disease. Med Clin North Am. 2010;94(1):135–53. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.mcna.2009.08.013.\nAlalawi M, Aljahdali S, Alharbi B, Fagih L, Fatani R, Aljuhani O. Clostridium difficile infection in an academic medical center in Saudi Arabia: prevalence and risk factors. Ann Saudi Med. 2020;40(4):305–9. https:\u002F\u002Fdoi.org\u002F10.5144\u002F0256-4947.2020.305.\nAl Otaibi H, Ahmed AE, Alammari M. Association between omeprazole use and Clostridium difficile infection among hospitalized patients: A case-control study of the Saudi population. Qatar Med J. 2017;2017(2):2. https:\u002F\u002Fdoi.org\u002F10.5339\u002Fqmj.2017.2.\nAlanazi MQ, Salam M, Alqahtani FY, Ahmed AE, Alenaze AQ, Al-Jeraisy M, et al. An evaluation of antibiotics prescribing patterns in the Emergency Department of a Tertiary Care Hospital in Saudi Arabia. Infect Drug Resist. 2019;12:3241–7. https:\u002F\u002Fdoi.org\u002F10.2147\u002FIDR.S211673.\nAl-Tawfiq JA, Momattin H, Hinedi K. Empiric antibiotic therapy in the treatment of community-acquired pneumonia in a General Hospital in Saudi Arabia. J Glob Infect Dis. 2019;11(2):69–72. https:\u002F\u002Fdoi.org\u002F10.4103\u002Fjgid.jgid_84_18.\nYu J, Wang G, Davidson A, Chow I, Chiu A. Antibiotics utilization for community acquired pneumonia in a Community Hospital Emergency Department. J Pharm Pract. 2020. https:\u002F\u002Fdoi.org\u002F10.1177\u002F0897190020953032.\nOrlando V, Monetti VM, Moreno Juste A, Russo V, Mucherino S, Trama U, et al. Drug utilization pattern of antibiotics: the role of age, sex and municipalities in determining variation. Risk ManagHealthc Policy. 2020;13:63–71. https:\u002F\u002Fdoi.org\u002F10.2147\u002FRMHP.S223042.\nPatra SK, Mishra SB, Rath A, Samal S, Iqbal SN. Study of antimicrobial utilization and cost of therapy in medicine intensive care unit of a tertiary care hospital in Eastern India. Indian J Crit Care Med. 2020;24(10):938–42. https:\u002F\u002Fdoi.org\u002F10.5005\u002Fjp-journals-10071-23552.\nTrikha S, Dalpath SK, Sharma M, Shafiq N. Antibiotic prescribing patterns and knowledge of antibiotic resistance amongst the doctors working at public health facilities of a state in northern India: a cross sectional study. J Family Med Prim Care. 2020;9(8):3937–43. https:\u002F\u002Fdoi.org\u002F10.4103\u002Fjfmpc.jfmpc_367_20.\nJarab AS, Mukattash TL, Nusairat B, Shawaqfeh M, Farha RA. Patterns of antibiotic use and administration in hospitalized patients in Jordan. Saudi Pharm J. 2018;26(6):764–70. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jsps.2018.04.009.\nAkdemIr Kalkan I, Cinar G, PehlIvanli A, Urkmez F, TopaloGlu IE, Akyol B, et al. Pattern of systemic antibiotic use and potential drug interactions: evaluations through a point prevalence study in Ankara University Hospitals. Turk J Med Sci. 2020. https:\u002F\u002Fdoi.org\u002F10.3906\u002Fsag-2004-164.\nThabit AK, Shea KM, Guzman OE, Garey KW. Antibiotic utilization within 18 community hospitals in the United States: A 5-year analysis. Pharmacoepidemiol Drug Saf. 2020. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fpds.5156.\nBrown KA, Khanafer N, Daneman N, Fisman DN. Meta-analysis of antibiotics and the risk of community-associated Clostridium difficile infection. Antimicrob Agents Chemother. 2013;57(5):2326–32. https:\u002F\u002Fdoi.org\u002F10.1128\u002FAAC.02176-12.\nDeshpande A, Pasupuleti V, Thota P, Pant C, Rolston DD, Sferra TJ, et al. Community-associated Clostridium difficile infection and antibiotics: a meta-analysis. J Antimicrob Chemother. 2013;68(9):1951–61. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fjac\u002Fdkt129.",{"VOID":1353},"10.1186\u002Fs13099-021-00405-9","2024-05-10T13:51:56.759+00:00","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-021-00405-9",[1357,1372],{"id":1358,"sortIndex":21,"researcher":20,"roles":1359,"affiliations":1360,"properties":1369,"displayName":1371,"givenName":20,"familyName":20},"7767ee10-0d11-4b3d-9621-4eaf8cc51dcb",[149],[1361],{"id":1362,"sortIndex":21,"affiliation":1363,"properties":20},"6f032e95-2a82-441d-9542-cee6bf82f724",{"id":1362,"createTime":20,"updateTime":20,"relativeEntities":1364,"slug":20,"properties":1365,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1368,"statistic":20},[],{"title":1366},{"VI":1367},"Pharmacy Practice Department, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia",[],{"title":1370},{"VI":1371},"Khadijah M. Alammari",{"id":1373,"sortIndex":112,"researcher":20,"roles":1374,"affiliations":1375,"properties":1382,"displayName":1384,"givenName":20,"familyName":20},"b34382e4-afcc-444b-9f5c-7e82564adaeb",[149],[1376],{"id":1362,"sortIndex":21,"affiliation":1377,"properties":20},{"id":1362,"createTime":20,"updateTime":20,"relativeEntities":1378,"slug":20,"properties":1379,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1381,"statistic":20},[],{"title":1380},{"VI":1367},[],{"title":1383},{"VI":1384},"Abrar K. 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The studies of the Campylobacter species thus far in all clinical isolates were to show the many kinds of antibiotic phenomenon that were produced. Their integrons cause the induction of antibiotic resistance between bacterial species in the Campylobacter species. The bacterial strains from the diarrhea of pediatric patient which isolated by China Medical University Hospital storage bank. These isolates were identified by MALDI-TOF mass spectrometry. The anti-microbial susceptibility test showed that Campylobacter species resistant to cefepime, streptomycin, tobramycin and trimethoprim\u002Fsulfamethoxazole (all C. jejuni and C. coli isolates), ampicillin (89% of C. jejuni; 75% of C. coli), cefotaxime (78% of C. jejuni; 100% of C. coli), nalidixic acid (78% of C. jejuni; 100% of C. coli), tetracycline (89% of C. jejuni; 25% C. coli), ciprofloxacin (67% of C. jejuni; 50% C. coli), kanamycin (33% of C. jejuni; 75% C. coli) and the C. fetus isolate resisted to ampicillin, cefotaxime, nalidixic acid, tetracycline, ciprofloxacin, kanamycin by disc-diffusion method. The effect for ciprofloxacin and tetracycline of the Campylobacter species was tested using an E-test. The tet, erm, and integron genes were detected by PCR assay. According to the sequencing analysis (type I: dfr12-gcuF-aadA2 genes and type II: dfrA7 gene), the cassette type was identified. The most common gene cassette type (type I: 9 C. jejuni and 2 C. coli isolates; type II: 1 C. coli isolates) was found in 12 class I integrase-positive isolates. Our results suggested an important information in the latency of Campylobacter species with resistance genes, and irrational antimicrobial use should be concerned.",{"EN":1462},"Class 1 integrons and plasmid-mediated multiple resistance genes of the Campylobacter species from pediatric patient of a university hospital in 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The consequences of Campylobacter infection. Curr Opin Gastroenterol. 2017;33(1):14–20.",{"doi":698},{"id":694,"text":1671,"url":696,"identifiers":1672},"Sahin O, Yaeger M, Wu Z, Zhang Q. Campylobacter-Associated Diseases in Animals. Annu Rev Anim Biosci 2017;5(21-42.",{"doi":698},{"id":694,"text":1674,"url":696,"identifiers":1675},"Skarp CP, Hanninen ML, Rautelin HI. Campylobacteriosis: the role of poultry meat. Clin Microbiol Infect. 2016;22(2):103–9.",{"doi":698},{"id":694,"text":1677,"url":696,"identifiers":1678},"Said B, Wright F, Nichols GL, Reacher M, Rutter M. Outbreaks of infectious disease associated with private drinking water supplies in England and Wales 1970–2000. Epidemiol Infect. 2003;130(3):469–79.",{"doi":698},{"id":1680,"text":1681,"url":1682,"identifiers":1683},"90997518-e5de-41c1-81c6-1fa738039bfc","Figueras MJ, Levican A, Collado L. Updated 16S rRNA-RFLP method for the identification of all currently characterised Arcobacter spp. BMC Microbiol. 2012;12:292.","http:\u002F\u002Fbmcmicrobiol.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2180-12-292",{"doi":1684},"10.1186\u002F1471-2180-12-292",{"id":20,"text":1686,"url":20,"identifiers":1687},"Wang Y, Dong Y, Deng F, Liu D, Yao H, Zhang Q, Shen J, Liu Z, Gao Y, Wu C, Shen Z. Species shift and multidrug resistance of Campylobacter from chicken and swine, China, 2008–2014. J Antimicrob Chemother. 2016;71(3):666–9.",{},{"id":20,"text":1689,"url":20,"identifiers":1690},"Fitzgerald C. Campylobacter. Clin Lab Med. 2015;35(2):289–98.",{},{"id":694,"text":1692,"url":696,"identifiers":1693},"Oosterom J. Campylobacter jejuni: an important causative agent of food infection in man. An overview. 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Biomed Res Int. 2013;2013:794643.",{"doi":698},{"id":694,"text":1740,"url":696,"identifiers":1741},"Ge B, Wang F, Sjolund-Karlsson M, McDermott PF. Antimicrobial resistance in Campylobacter: susceptibility testing methods and resistance trends. J Microbiol Methods. 2013;95(1):57–67.",{"doi":698},{"id":694,"text":1743,"url":696,"identifiers":1744},"Abdi-Hachesoo B, Khoshbakht R, Sharifiyazdi H, Tabatabaei M, Hosseinzadeh S, Asasi K. Tetracycline resistance genes in Campylobacter jejuni and C. coli isolated from poultry carcasses. Jundishapur J Microbiol. 2014;7(9):e12129.",{"doi":698},{"id":694,"text":1746,"url":696,"identifiers":1747},"Mottola C, Matias CS, Mendes JJ, Melo-Cristino J, Tavares L, Cavaco-Silva P, Oliveira M. Susceptibility patterns of Staphylococcus aureus biofilms in diabetic foot infections. BMC Microbiol. 2016;16(1):119.",{"doi":698},{"id":694,"text":1749,"url":696,"identifiers":1750},"Lindstedt BA, Heir E, Nygard I, Kapperud G. Characterization of class I integrons in clinical strains of Salmonella enterica subsp. enterica serovars Typhimurium and Enteritidis from Norwegian hospitals. J Med Microbiol. 2003;52(Pt 2):141–9.",{"doi":698},{"id":694,"text":1752,"url":696,"identifiers":1753},"Ng LK, Mulvey MR, Martin I, Peters GA, Johnson W. Genetic characterization of antimicrobial resistance in Canadian isolates of Salmonella serovar Typhimurium DT104. Antimicrob Agents Chemother. 1999;43(12):3018–21.",{"doi":698},{"id":1755,"text":1756,"url":1757,"identifiers":1758},"ac015f97-f719-4df3-a161-9fee7d6f041a","Tenover FC, Arbeit RD, Goering RV, Mickelsen PA, Murray BE, Persing DH, Swaminathan B. Interpreting chromosomal DNA restriction patterns produced by pulsed-field gel electrophoresis: criteria for bacterial strain typing. J Clin Microbiol. 1995;33(9):2233–9.","https:\u002F\u002Fjournals.asm.org\u002Fdoi\u002F10.1128\u002Fjcm.33.9.2233-2239.1995",{"doi":1759},"10.1128\u002Fjcm.33.9.2233-2239.1995",{"id":694,"text":1761,"url":696,"identifiers":1762},"Wieczorek K, Osek J. Antimicrobial resistance mechanisms among Campylobacter. Biomed Res Int. 2013;2013:340605.",{"doi":698},{"id":694,"text":1764,"url":696,"identifiers":1765},"Gibreel A, Tracz DM, Nonaka L, Ngo TM, Connell SR, Taylor DE. Incidence of antibiotic resistance in Campylobacter jejuni isolated in Alberta, Canada, from 1999 to 2002, with special reference to tet(O)-mediated tetracycline resistance. Antimicrob Agents Chemother. 2004;48(9):3442–50.",{"doi":698},{"id":694,"text":1767,"url":696,"identifiers":1768},"Qin S, Wang Y, Zhang Q, Zhang M, Deng F, Shen Z, Wu C, Wang S, Zhang J, Shen J. Report of ribosomal RNA methylase gene erm(B) in multidrug-resistant Campylobacter coli. J Antimicrob Chemother. 2014;69(4):964–8.",{"doi":698},{"id":694,"text":1770,"url":696,"identifiers":1771},"Wang Y, Zhang M, Deng F, Shen Z, Wu C, Zhang J, Zhang Q, Shen J. Emergence of multidrug-resistant Campylobacter species isolates with a horizontally acquired rRNA methylase. Antimicrob Agents Chemother. 2014;58(9):5405–12.",{"doi":698},{"id":694,"text":1773,"url":696,"identifiers":1774},"Lee MD, Sanchez S, Zimmer M, Idris U, Berrang ME, McDermott PF. Class 1 integron-associated tobramycin-gentamicin resistance in Campylobacter jejuni isolated from the broiler chicken house environment. Antimicrob Agents Chemother. 2002;46(11):3660–4.",{"doi":698},{"id":1776,"createTime":1777,"updateTime":1778,"relativeEntities":1779,"slug":1780,"properties":1781,"entityType":140,"verifyStatus":141,"verifyTime":1778,"verifyNote":143,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1790,"fullTextUrl":20,"authors":1791,"publicationType":341,"publisherRelationship":1807,"citationCount":20,"citationInfo":20,"publishDate":1869,"publishYear":1870,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1871,"openAccess":20,"references":20,"isForceReanalyzing":413},"ff33e28a-594f-4fa5-b516-ff6955645663","2024-01-01T10:43:44.090+00:00","2025-02-26T19:37:26.945+00:00",[],"De-Novo-sphingolipid-synthesis-is-essential-for-Salmonella-induced-autophagy-and-human-beta-defensin-2-expression-in-intestinal-epithelial-cells",{"abstract":1782,"title":1784,"references":1786,"doi":1788},{"EN":1783},"Sphingolipids are important for innate immune response to eliminate infected pathogens and involved in autophagy. On the other hand, nucleotide-binding oligomerization domain-containing protein 2 (NOD2) served as an intracellular pattern recognition receptor to enhance host defense by inducing autophagy and the production of antimicrobial peptides, such as human beta-defensin-2 (hBD-2). However, the role of sphingolipids in Salmonella-induced autophagy and hBD-2 response in intestinal epithelial cells has not been previously elucidated. \n                           Salmonella typhimurium wild-type strain SL1344 was used to infect SW480, an intestinal epithelial cell. hBD-2 and interleukin-8 (IL-8) mRNA expressions were assessed in SW480 cells using RT-PCR, and intracellular signaling pathways and autophagy protein expression were analyzed by Western blot in SW480 cells in the presence or absence of inhibitors or transfected with siRNA. We demonstrated that inhibition of de novo sphingolipid synthesis repressed the membrane recruitment of NOD2 and autophagy-related protein 16-like 1 (Atg16L1), suppressed Salmonella-induced autophagic protein LC3-II expression, and reduced NOD2-mediated hBD-2 response in Salmonella-infected SW480 cells. Contrasting to the utilization of membrane cholesterol on maintenance of Salmonella-containing vacuoles and anti-inflammation by Salmonella, sphingolipids act on epithelial defense against the invasive pathogen. Our results offer mechanistic insights on the role of de novo sphingolipid synthesis in the innate immunity of intestinal epithelial cells to Salmonella infection. The pharmaceuticals enhancing or diet enriched with sphingolipids may induce the dual anti-bacterial mechanisms. The role of de novo sphingolipid synthesis on inflammatory bowel disease is deserved to be further investigated.",{"EN":1785},"De Novo sphingolipid synthesis is essential for Salmonella-induced autophagy and human beta-defensin 2 expression in intestinal epithelial cells",{"VOID":1787},"Gulbins E, Dreschers S, Wilker B, Grassme H. Ceramide, membrane rafts and infections. J Mol Med (Berl). 2004;82(6):357–63. doi:10.1007\u002Fs00109-004-0539-y.\nGrassme H, Jendrossek V, Riehle A, von Kurthy G, Berger J, Schwarz H, et al. Host defense against Pseudomonas aeruginosa requires ceramide-rich membrane rafts. Nat Med. 2003;9(3):322–30. doi:10.1038\u002Fnm823.17.\nHanada K. Sphingolipids in infectious diseases. Jpn J Infect Dis. 2005;58(3):131–48.\nJiang W, Ogretmen B. Autophagy paradox and ceramide. Biochim Biophys Acta. 2014;1841(5):783–92. doi:10.1016\u002Fj.bbalip.2013.09.005.\nPark JW, Park WJ, Futerman AH. Ceramide synthases as potential targets for therapeutic intervention in human diseases. Biochim Biophys Acta. 2014;1841(5):671–81. doi:10.1016\u002Fj.bbalip.2013.08.019.\nYamagata M, Obara K, Kihara A. Sphingolipid synthesis is involved in autophagy in Saccharomyces cerevisiae. Biochem Biophys Res Commun. 2011;410(4):786–91. doi:10.1016\u002Fj.bbrc.2011.06.061.\nTravassos LH, Carneiro LA, Ramjeet M, Hussey S, Kim YG, Magalhaes JG, et al. Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry. Nat Immunol. 2010;11(1):55–62. doi:10.1038\u002Fni.1823.\nCooney R, Baker J, Brain O, Danis B, Pichulik T, Allan P, et al. NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation. Nat Med. 2010;16(1):90–7. doi:10.1038\u002Fnm.2069.\nVoss E, Wehkamp J, Wehkamp K, Stange EF, Schroder JM, Harder J. NOD2\u002FCARD15 mediates induction of the antimicrobial peptide human beta-defensin-2. J Biol Chem. 2006;281(4):2005–11. doi:10.1074\u002Fjbc.M511044200.\nHuang GT, Zhang HB, Kim D, Liu L, Ganz T. A model for antimicrobial gene therapy: demonstration of human beta-defensin 2 antimicrobial activities in vivo. Hum Gene Ther. 2002;13(17):2017–25. doi:10.1089\u002F10430340260395875.\nLasserre R, Guo XJ, Conchonaud F, Hamon Y, Hawchar O, Bernard AM, et al. Raft nanodomains contribute to Akt\u002FPKB plasma membrane recruitment and activation. Nat Chem Biol. 2008;4(9):538–47. doi:10.1038\u002Fnchembio.103.\nKnodler LA, Finlay BB, Steele-Mortimer O. The Salmonella effector protein SopB protects epithelial cells from apoptosis by sustained activation of Akt. J Biol Chem. 2005;280(10):9058–64. doi:10.1074\u002Fjbc.M412588200.18.\nBirmingham CL, Brumell JH. Autophagy recognizes intracellular Salmonella enterica serovar Typhimurium in damaged vacuoles. Autophagy. 2006;2(3):156–8.\nHuang FC. The critical role of membrane cholesterol in salmonella-induced autophagy in intestinal epithelial cells. Int J Mol Sci. 2014;15(7):12558–72. doi:10.3390\u002Fijms150712558.\nYoung MM, Kester M, Wang HG. Sphingolipids: regulators of crosstalk between apoptosis and autophagy. J Lipid Res. 2013;54(1):5–19. doi:10.1194\u002Fjlr.R031278.\nPoole K, Meder D, Simons K, Muller D. The effect of raft lipid depletion on microvilli formation in MDCK cells, visualized by atomic force microscopy. FEBS Lett. 2004;565(1–3):53–8. doi:10.1016\u002Fj.febslet.2004.03.095.\nSchwan C, Nolke T, Kruppke AS, Schubert DM, Lang AE, Aktories K. Cholesterol- and sphingolipid-rich microdomains are essential for microtubule-based membrane protrusions induced by Clostridium difficile transferase (CDT). J Biol Chem. 2011;286(33):29356–65. doi:10.1074\u002Fjbc.M111.261925.\nHidari K, Ichikawa S, Fujita T, Sakiyama H, Hirabayashi Y. Complete removal of sphingolipids from the plasma membrane disrupts cell to substratum adhesion of mouse melanoma cells. J Biol Chem. 1996;271(24):14636–41.\nBarnich N, Aguirre JE, Reinecker HC, Xavier R, Podolsky DK. Membrane recruitment of NOD2 in intestinal epithelial cells is essential for nuclear factor-{kappa}B activation in muramyl dipeptide recognition. J Cell Biol. 2005;170(1):21–6. doi:10.1083\u002Fjcb.200502153.\nGulbins E, Bissonnette R, Mahboubi A, Martin S, Nishioka W, Brunner T, et al. FAS-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway. Immunity. 1995;2(4):341–51.\nVerheij M, Bose R, Lin XH, Yao B, Jarvis WD, Grant S, et al. Requirement for ceramide-initiated SAPK\u002FJNK signalling in stress-induced apoptosis. Nature. 1996;380(6569):75–9. doi:10.1038\u002F380075a0.\nHuang FC, Li Q, Cherayil BJ. A phosphatidyl-inositol-3-kinase-dependent anti-inflammatory pathway activated by Salmonella in epithelial cells. FEMS Microbiol Lett. 2005;243(1):265–70. doi:10.1016\u002Fj.femsle.2004.12.013.19.\nSanjuan MA, Milasta S, Green DR. Toll-like receptor signaling in the lysosomal pathways. Immunol Rev. 2009;227(1):203–20. doi:10.1111\u002Fj.1600-065X.2008.00732.x.\nHomer CR, Richmond AL, Rebert NA, Achkar JP, McDonald C. ATG16L1 and NOD2 interact in an autophagy-dependent antibacterial pathway implicated in Crohn’s disease pathogenesis. Gastroenterology. 2010;139(5):1630–41. doi:10.1053\u002Fj.gastro.2010.07.006 (e1–2).\nConway KL, Kuballa P, Song JH, Patel KK, Castoreno AB, Yilmaz OH, et al. Atg16l1 is Required for Autophagy in Intestinal Epithelial Cells and Protection of Mice from Salmonella Infection. Gastroenterology. 2013;. doi:10.1053\u002Fj.gastro.2013.08.035.\nOswald IP, Desautels C, Laffitte J, Fournout S, Peres SY, Odin M, et al. Mycotoxin fumonisin B1 increases intestinal colonization by pathogenic Escherichia coli in pigs. Appl Environ Microbiol. 2003;69(10):5870–4.\nLapaquette P, Darfeuille-Michaud A. Abnormalities in the handling of intracellular bacteria in Crohn’s disease. J Clin Gastroenterol. 2010;44(Suppl 1):S26–9. doi:10.1097\u002FMCG.0b013e3181dd4fa5.\nKuballa P, Huett A, Rioux JD, Daly MJ, Xavier RJ. Impaired autophagy of an intracellular pathogen induced by a Crohn’s disease associated ATG16L1 variant. PLoS One. 2008;3(10):e3391. doi:10.1371\u002Fjournal.pone.0003391.\nKurek K, Lukaszuk B, Piotrowska DM, Wiesiolek P, Chabowska AM, Zendzian-Piotrowska M. Metabolism, physiological role, and clinical implications of sphingolipids in gastrointestinal tract. BioMed Res Int. 2013;2013:908907. doi:10.1155\u002F2013\u002F908907.\nJess T, Simonsen J, Nielsen NM, Jorgensen KT, Bager P, Ethelberg S, et al. Enteric Salmonella or Campylobacter infections and the risk of inflammatory bowel disease. Gut. 2011;60(3):318–24. doi:10.1136\u002Fgut.2010.223396.\nAbraham C, Medzhitov R. Interactions between the host innate immune system and microbes in inflammatory bowel disease. Gastroenterology. 2011;140(6):1729–37. doi:10.1053\u002Fj.gastro.2011.02.012.\nAldhous MC, Noble CL, Satsangi J. Dysregulation of human beta-defensin-2 protein in inflammatory bowel disease. PLoS One. 2009;4(7):e6285. doi:10.1371\u002Fjournal.pone.0006285.20.\nZilbauer M, Jenke A, Wenzel G, Postberg J, Heusch A, Phillips AD, et al. Expression of human beta-defensins in children with chronic inflammatory bowel disease. PLoS One. 2010;5(10):e15389. doi:10.1371\u002Fjournal.pone.0015389.\nDaniel C, Sartory N, Zahn N, Geisslinger G, Radeke HH, Stein JM. FTY720 ameliorates Th1-mediated colitis in mice by directly affecting the functional activity of CD4 + CD25 + regulatory T cells. J Immunol. 2007;178(4):2458–68.\nBrown DA, London E. Structure and function of sphingolipid- and cholesterol-rich membrane rafts. J Biol Chem. 2000;275(23):17221–4. doi:10.1074\u002Fjbc.R000005200.\nHelms JB, Zurzolo C. Lipids as targeting signals: lipid rafts and intracellular trafficking. Traffic. 2004;5(4):247–54. doi:10.1111\u002Fj.1600-0854.2004.0181.x.\nHuang FC. Plasma membrane cholesterol plays a critical role in the Salmonella-induced anti-inflammatory response in intestinal epithelial cells. Cell Immunol. 2011;271(2):480–7. doi:10.1016\u002Fj.cellimm.2011.08.018.\nMao-Qiang M, Feingold KR, Elias PM. Inhibition of cholesterol and sphingolipid synthesis causes paradoxical effects on permeability barrier homeostasis. J Invest Dermatol. 1993;101(2):185–90.\nHuang FC. Regulation of Salmonella flagellin-induced interleukin-8 in intestinal epithelial cells by muramyl dipeptide. Cell Immunol. 2012;278(1–2):1–9. doi:10.1016\u002Fj.cellimm.2012.06.013.\nHuang FC. Differential regulation of interleukin-8 and human beta-defensin 2 in Pseudomonas aeruginosa -infected intestinal epithelial cells. BMC Microbiol. 2014;14(1):275. doi:10.1186\u002Fs12866-014-0275-6.",{"VOID":1789},"10.1186\u002Fs13099-016-0088-2","https:\u002F\u002Fgutpathogens.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13099-016-0088-2",[1792],{"id":1793,"sortIndex":21,"researcher":20,"roles":1794,"affiliations":1795,"properties":1804,"displayName":1806,"givenName":20,"familyName":20},"1ead234f-6d5a-47d9-a477-c7b3a22744c1",[149],[1796],{"id":1797,"sortIndex":21,"affiliation":1798,"properties":20},"15c12a0f-103c-4f6e-a95d-e86a1249dc3f",{"id":1797,"createTime":20,"updateTime":20,"relativeEntities":1799,"slug":20,"properties":1800,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1803,"statistic":20},[],{"title":1801},{"VI":1802},"Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan",[],{"title":1805},{"VI":1806},"Fu-Chen Huang",{"url":1790,"publisher":1808,"properties":1865},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1809,"slug":10,"properties":1810,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1813,"manageAffiliations":1834,"indexDatabases":1845,"url":20,"thumbnailPath":20,"statistic":1860,"gsStatistic":20,"type":118,"analyzePriority":20},[],{"issn":1811,"title":1812},{"VOID":13},{"EN":15},[1814,1818,1822,1826,1830],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1815,"label":1816,"description":1817,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1819,"label":1820,"description":1821,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":1823,"label":1824,"description":1825,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":1827,"label":1828,"description":1829,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},{"id":48,"createTime":20,"updateTime":20,"relativeEntities":1831,"label":1832,"description":1833,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":51},{},[1835,1840],{"id":55,"createTime":20,"updateTime":20,"relativeEntities":1836,"slug":20,"properties":1837,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1839,"statistic":20},[],{"title":1838},{"EN":59},[],{"id":62,"createTime":20,"updateTime":20,"relativeEntities":1841,"slug":20,"properties":1842,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1844,"statistic":20},[],{"title":1843},{"EN":66},[],[1846,1853],{"id":70,"indexDatabase":1847,"url":83,"indexYears":20,"academicFieldIds":1852,"indexDatabaseRanking":20},{"id":72,"createTime":20,"updateTime":20,"relativeEntities":1848,"label":1849,"description":1850,"key":79,"publicationTags":1851,"standard":20},[],{"EN":75,"VI":75},{"EN":77,"VI":78},[81,82],[85,86],{"id":88,"indexDatabase":1854,"url":99,"indexYears":100,"academicFieldIds":1859,"indexDatabaseRanking":107},{"id":90,"createTime":20,"updateTime":20,"relativeEntities":1855,"label":1856,"description":1857,"key":96,"publicationTags":1858,"standard":20},[],{"EN":93,"VI":93},{"EN":93,"VI":95},[98],[102,103,104,105,106],{"impactFactor":21,"impactFactorByYear":1861,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":110,"totalPublicationByYear":1862,"totalCitation":21,"totalCitationByYear":1863,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":1864,"hindexLast5Year":21,"hindex":21},{},{"2011":112,"2013":112,"2014":112,"2016":112,"2018":112,"2019":112,"2020":112,"2021":113,"2023":114,"2024":115},{},{},{"pages":1866,"volume":1867},{"VOID":1051},{"VOID":1868},"8","2016-02-18",2016,[107,81],{"id":1873,"createTime":1874,"updateTime":1875,"relativeEntities":1876,"slug":1877,"properties":1878,"entityType":140,"verifyStatus":141,"verifyTime":1875,"verifyNote":143,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1887,"fullTextUrl":20,"authors":1888,"publicationType":341,"publisherRelationship":1972,"citationCount":20,"citationInfo":20,"publishDate":2033,"publishYear":1870,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":2034,"openAccess":20,"references":20,"isForceReanalyzing":413},"9687d65c-04bf-453d-b50f-d8044dc0c2b8","2024-01-10T10:33:23.047+00:00","2025-02-26T18:46:14.207+00:00",[],"Interferon-%CE%B3-promotes-gastric-lymphoid-follicle-formation-but-not-gastritis-in-Helicobacter-infected-BALB-c-mice",{"abstract":1879,"title":1881,"references":1883,"doi":1885},{"EN":1880},"Mouse infection studies have shown that interferon-γ (IFN-γ), a T helper 1 (Th1) cytokine, is required for the development of severe pathology induced by chronic Helicobacter infection. This finding is largely based on studies performed using mice that have polarised Th1 responses i.e. C57BL\u002F6 animals. The current work aims to investigate the role of IFN-γ in Helicobacter-induced inflammation in BALB\u002Fc mice which have Th2-polarised immune responses. At 7 months post-infection with Helicobacter felis, IFN-γ deficiency in BALB\u002Fc mice had no significant effect on H. felis colonisation levels in the gastric mucosa, nor on humoral responses, or gastritis severity. Ifng\n                           −\u002F− animals with chronic H. felis infection did, however, develop significantly fewer lymphoid follicle lesions, as well as increased IL-4 splenocyte responses, when compared with infected Ifng\n                           +\u002F+ mice (P = 0.015 and P = 0.0004, respectively). The work shows that in mice on a BALB\u002Fc background, IFN-γ is not required for bacterial clearance, antibody responses, nor gastric inflammation. Conversely, IFN-γ appears to play a role in the development of gastric lymphoid follicles, which are precursor lesions to mucosa-associated lymphoid tissue (MALT) lymphoma. This study highlights the importance of mouse host background on the susceptibility to Helicobacter-induced pathologies.",{"EN":1882},"Interferon-γ promotes gastric lymphoid follicle formation but not gastritis in Helicobacter-infected BALB\u002Fc mice",{"VOID":1884},"Correa P, Houghton J. Carcinogenesis of Helicobacter pylori. Gastroenterology. 2007;133(2):659–72.\nKarttunen R, Karttunen T, Ekre HP, MacDonald TT. Interferon gamma and interleukin 4 secreting cells in the gastric antrum in Helicobacter pylori positive and negative gastritis. Gut. 1995;36(3):341–5.\nMohammadi M, Czinn S, Redline R, Nedrud J. Helicobacter-specific cell-mediated immune responses display a predominant Th1 phenotype and promote a delayed-type hypersensitivity response in the stomachs of mice. J Immunol. 1996;156(12):4729–38.\nSawai N, Kita M, Kodama T, Tanahashi T, Yamaoka Y, Tagawa Y, Iwakura Y, Imanishi J. Role of gamma interferon in Helicobacter pylori-induced gastric inflammatory responses in a mouse model. Infect Immun. 1999;67(1):279–85.\nBamford KB, Fan X, Crowe SE, Leary JF, Gourley WK, Luthra GK, Brooks EG, Graham DY, Reyes VE, Ernst PB. Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype. Gastroenterology. 1998;114(3):482–92.\nD’Elios MM, Amedei A, Manghetti M, Costa F, Baldari CT, Quazi AS, Telford JL, Romagnani S, Del Prete G. Impaired T-cell regulation of B-cell growth in Helicobacter pylori–related gastric low-grade MALT lymphoma. Gastroenterology. 1999;117(5):1105–12.\nEaton KA, Mefford M, Thevenot T. The role of T cell subsets and cytokines in the pathogenesis of Helicobacter pylori gastritis in mice. J Immunol. 2001;166(12):7456–61.\nPellicanò A, Sebkova L, Monteleone G, Guarnieri G, Imeneo M, Pallone F, Luzza F. Interleukin-12 drives the Th1 signaling pathway in Helicobacter pylori-infected human gastric mucosa. Infect Immun. 2007;75(4):1738–44.\nSmythies LE, Waites KB, Lindsey JR, Harris PR, Ghiara P, Smith PD. Helicobacter pylori-induced mucosal inflammation is Th1 mediated and exacerbated in IL-4, but not IFN-gamma, gene-deficient mice. J Immunol. 2000;165(2):1022–9.\nGarhart CA, Nedrud JG, Heinzel FP, Sigmund NE, Czinn SJ. Vaccine-induced protection against Helicobacter pylori in mice lacking both antibodies and interleukin-4. Infect Immun. 2003;71(6):3628–33.\nLucas B, Bumann D, Walduck A, Koesling J, Develioglu L, Meyer TF, Aebischer T. Adoptive transfer of CD4 + T Cells specific for subunit A of Helicobacter pylori urease reduces H. pylori stomach colonization in mice in the absence of interleukin-4 (IL-4)\u002FIL-13 receptor signaling. Infect Immun. 2001;69(3):1714–21.\nSaldinger PF, Porta N, Launois P, Louis JA, Waanders GA, Bouzourène H, Michetti P, Blum AL, Corthésy-Theulaz IE. Immunization of BALB\u002Fc mice with Helicobacter urease B induces a T helper 2 response absent in Helicobacter infection. Gastroenterology. 1998;115(4):891–7.\nSayi A, Kohler E, Hitzler I, Arnold I, Schwendener R, Rehrauer H, Müller A. The CD4 + T cell-mediated IFN-γ response to Helicobacter infection is essential for clearance and determines gastric cancer risk. J Immunol. 2009;182(11):7085–101.\nBerg DJ, Lynch NA, Lynch RG, Lauricella DM. Rapid development of severe hyperplastic gastritis with gastric epithelial dedifferentiation in Helicobacter felis-infected IL-10−\u002F− mice. Am J Pathol. 1998;152(5):1377–86.\nCai X, Carlson J, Stoicov C, Li H, Wang TC, Houghton J. Helicobacter felis eradication restores normal architecture and inhibits gastric cancer progression in C57BL\u002F6 mice. Gastroenterol. 2005;128(7):1937–52.\nEnno A, O’Rourke JL, Howlett CR, Jack A, Dixon MF, Lee A. MALToma-like lesions in the murine gastric mucosa after long-term infection with Helicobacter felis. A mouse model of Helicobacter pylori-induced gastric lymphoma. Am J Pathol. 1995;147(1):217–22.\nLee JY, Kim N, Choi YJ, Nam RH, Choi YJ, Kwon YH, Yoon K, Suh JH, Lee SM, Lee HS, et al. Histologic findings and inflammatory reactions after long-term colonization of Helicobacter felis in C57BL\u002F6 mice. J Cancer Prev. 2014;19(3):224–30.\nRoth KA, Kapadia SB, Martin SM, Lorenz RG. Cellular immune responses are essential for the development of Helicobacter felis-associated gastric pathology. J Immunol. 1999;163(3):1490–7.\nLee A, O’Rourke J, De Ungria MC, Robertson B, Daskalopoulos G, Dixon MF. A standardized mouse model of Helicobacter pylori infection: introducing the Sydney strain. 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Microbes Infect. 2000;2(6):593–7.\nSakagami T, Dixon M, O’Rourke J, Howlett R, Alderuccio F, Vella J, Shimoyama T, Lee A. Atrophic gastric changes in both Helicobacter felis and Helicobacter pylori infected mice are host dependent and separate from antral gastritis. Gut. 1996;39(5):639–48.\nEnno A, O’Rourke J, Braye S, Howlett R, Lee A. Antigen-dependent progression of mucosa-associated lymphoid tissue (MALT)-type lymphoma in the stomach. Effects of antimicrobial therapy on gastric MALT lymphoma in mice. Am J Pathol. 1998;152(6):1625–32.\nMohammadi M, Nedrud J, Redline R, Lycke N, Czinn SJ. Murine CD4 T-cell response to Helicobacter infection: tH1 cells enhance gastritis and TH2 cells reduce bacterial load. Gastroenterology. 1997;113(6):1848–57.\nFerrero RL, Thiberge J-M, Labigne A. Local immunoglobulin G antibodies in the stomach may contribute to immunity against Helicobacter infection in mice. Gastroenterology. 1997;113:185–94.\nFerrero RL, Ave P, Ndiaye D, Bambou JC, Huerre MR, Philpott DJ, Memet S. NF-kappaB activation during acute Helicobacter pylori infection in mice. Infect Immun. 2008;76(2):551–61.\nViala J, Chaput C, Boneca IG, Cardona A, Girardin SE, Moran AP, Athman R, Mémet S, Huerre MR, Coyle AJ, et al. Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island. Nat Immunol. 2004;51:166–74.\nSutton P, Wilson J, Genta R, Torrey D, Savinainen A, Pappo J, Lee A. A genetic basis for atrophy: dominant non-responsiveness and Helicobacter induced gastritis in F(1) hybrid mice. Gut. 1999;45(3):335–40.\nHuang S, Hendriks W, Althage A, Hemmi S, Bluethmann H, Kamijo R, Vilcek J, Zinkernagel RM, Aguet M. Immune response in mice that lack the interferon-gamma receptor. Science. 1993;259(5102):1742–5.\nCollins JT, Dunnick WA. Germline transcripts of the murine immunoglobulin gamma 2a gene: structure and induction by IFN-gamma. 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Interferon-gamma-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection. Muc Immunol. 2015;8(2):279–95.\nRad R, Dossumbekova A, Neu B, Lang R, Bauer S, Saur D, Gerhard M, Prinz C. Cytokine gene polymorphisms influence mucosal cytokine expression, gastric inflammation, and host specific colonisation during Helicobacter pylori infection. Gut. 2004;53(8):1082–9.\nWang SK, Zhu HF, He BS, Zhang ZY, Chen ZT, Wang ZZ, Wu GL. CagA + H. pylori infection is associated with polarization of T helper cell immune responses in gastric carcinogenesis. World J Gastroenterol. 2007;13(21):2923–31.\nRiedel S, Kraft M, Kucharzik T, Pauels HG, Tiemann M, Steinbuchel A, Domschke W, Lugering N. CD4 + Th1-cells predominate in low-grade B-cell lymphoma of gastric mucosa-associated lymphoid tissue (MALT type). Scand J Gastroenterol. 2001;36(11):1198–203.\nShi Y, Liu XF, Zhuang Y, Zhang JY, Liu T, Yin Z, Wu C, Mao XH, Jia KR, Wang FJ, et al. 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Reciprocal IFN-gamma and TGF-beta responses regulate the occurrence of mucosal inflammation. Immunol Today. 1997;18(2):61–4.\nDhiman N, Ovsyannikova IG, Ryan JE, Jacobson RM, Vierkant RA, Pankratz VS, Jacobsen SJ, Poland GA. Correlations among measles virus-specific antibody, lymphoproliferation and Th1\u002FTh2 cytokine responses following measles-mumps-rubella-II (MMR-II) vaccination. Clin Exp Immunol. 2005;142(3):498–504.\nBergman MP, D’Elios MM. Cytotoxic T cells in H. pylori-related gastric autoimmunity and gastric lymphoma. J Biomed Biotechnol. 2010;2010:104–918.\nCraig VJ, Cogliatti SB, Arnold I, Gerke C, Balandat JE, Wundisch T, Muller A. B-cell receptor signaling and CD40 ligand-independent T cell help cooperate in Helicobacter-induced MALT lymphomagenesis. Leukemia. 2010;24(6):1186–96.\nHussell T, Isaacson PG, Crabtree JE, Spencer J. Helicobacter pylori-specific tumour-infiltrating T cells provide contact dependent help for the growth of malignant B cells in low-grade gastric lymphoma of mucosa-associated lymphoid tissue. J Pathol. 1996;178(2):122–7.\nO’Rourke JL, Dixon MF, Jack A, Enno A, Lee A. Gastric B-cell mucosa-associated lymphoid tissue (MALT) lymphoma in an animal model of ‘Helicobacter heilmannii’ infection. J Pathol. 2004;203(4):896–903.\nHauer AC, Finn TM, MacDonald TT, Spencer J, Isaacson PG. Analysis of TH1 and TH2 cytokine production in low grade B cell gastric MALT-type lymphomas stimulated in vitro with Helicobacter pylori. J Clin Pathol. 1997;50(11):957–9.\nMueller A, O’Rourke J, Chu P, Chu A, Dixon MF, Bouley DM, Lee A, Falkow S. The role of antigenic drive and tumor-Infiltrating accessory cells in the pathogenesis of Helicobacter-induced mucosa-associated lymphoid tissue lymphoma. 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