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Mycobacterium massiliense gây ra phản ứng viêm ở đại thực bào thông qua thụ thể Toll-Like 2 và c-Jun N-Terminal Kinase
Tóm tắt
Mycobacterium massiliense (Mmass) là một loại mycobacterium đang nổi lên, phát triển nhanh (RGM) thuộc nhóm M. abscessus (Mabc), mặc dù rõ ràng khác biệt so với Mabc. So với M. tuberculosis, một tác nhân gây bệnh ở người đã được định hình rõ ràng, phản ứng miễn dịch bẩm sinh của chủ thể đối với nhiễm trùng Mmass vẫn còn chưa được biết đến nhiều. Trong nghiên cứu này, chúng tôi cho thấy Mmass kích hoạt mạnh mẽ sự biểu hiện mRNA và protein của yếu tố hoại tử khối u (TNF)-α và interleukin (IL)-6 trong các đại thực bào (BMDMs) lấy từ tủy xương chuột. Thụ thể Toll-like (TLR)-2 và gen phản ứng chính phân chia bạch cầu 88 (MyD88), nhưng không phải TLR4 hay Dectin-1, đều tham gia vào việc sản xuất TNF-α hoặc IL-6 do Mmass gây ra ở BMDMs. Nhiễm trùng Mmass cũng kích hoạt con đường kinase hoạt hóa bởi mitogen (MAPKs; c-Jun N-terminal kinase (JNK), ERK1/2 và p38 MAPK). Sự sản xuất TNF-α và IL-6 do Mmass gây ra phụ thuộc vào hoạt hóa JNK, trong khi không bị ảnh hưởng bởi con đường ERK1/2 hay p38 ở BMDMs. Thêm vào đó, các loài oxy phản ứng (ROS) nội bào, NADPH oxidase-2, và yếu tố hạt nhân-κB là cần thiết cho việc sản xuất cytokine gây viêm do Mmass gây ra ở các đại thực bào. Hơn nữa, kiểu hình S của Mmass cho thấy sự kích thích tổng thể của các cytokine pro-inflammation (TNF-α, IL-6, và IL-1β) và anti-inflammation (IL-10) thấp hơn so với kiểu hình R, cho thấy tính chất miễn dịch ít hơn đối với chủng lâm sàng này. Tổng thể, các kết quả này gợi ý rằng sự hoạt hóa các cytokine pro-inflammation ở chủ thể do Mmass gây ra được trung gian thông qua con đường tín hiệu TLR2 phụ thuộc vào JNK và ROS.
Từ khóa
#Mycobacterium massiliense #đại thực bào #thụ thể Toll-Like 2 #yếu tố hoại tử khối u TNF-α #interleukin-6 #con đường MAPK #phản ứng viêmTài liệu tham khảo
Marras TK, Daley CL. Epidemiology of human pulmonary infection with nontuberculous mycobacteria. Clin Chest Med. 2002;23(3):553–67.
Thibault VC, Grayon M, Boschiroli ML, Hubbans C, Overduin P, Stevenson K, et al. New variable-number tandem-repeat markers for typing Mycobacterium avium subsp. paratuberculosis and M. avium strains: comparison with IS900 and IS1245 restriction fragment length polymorphism typing. J Clin Microbiol. 2007;45(8):2404–10.
Inagaki T, Nishimori K, Yagi T, Ichikawa K, Moriyama M, Nakagawa T, et al. Comparison of a variable-number tandem-repeat (VNTR) method for typing Mycobacterium avium with mycobacterial interspersed repetitive-unit-VNTR and IS1245 restriction fragment length polymorphism typing. J Clin Microbiol. 2009;47(7):2156–64.
Choi GE, Chang CL, Whang J, Kim HJ, Kwon OJ, Koh WJ, et al. Efficient differentiation of Mycobacterium abscessus complex isolates to the species level by a novel PCR-based variable-number tandem-repeat assay. J Clin Microbiol. 2011;49(3):1107–9.
Zelazny AM, Root JM, Shea YR, Colombo RE, Shamputa IC, Stock F, et al. Cohort study of molecular identification and typing of Mycobacterium abscessus, Mycobacterium massiliense, and Mycobacterium bolletii. J Clin Microbiol. 2009;47(7):1985–95.
Koh WJ, Jeon K, Lee NY, Kim BJ, Kook YH, Lee SH, et al. Clinical significance of differentiation of Mycobacterium massiliense from Mycobacterium abscessus. Am J Respir Crit Care Med. 2011;183(3):405–10.
Huynh KK, Joshi SA, Brown EJ. A delicate dance: host response to mycobacteria. Curr Opin Immunol. 2011;23(4):464–72.
Jo EK, Park JK, Dockrell HM. Dynamics of cytokine generation in patients with active pulmonary tuberculosis. Curr Opin Infect Dis. 2003;16(3):205–10.
Stenger S. Immunological control of tuberculosis: role of tumour necrosis factor and more. Ann Rheum Dis. 2005;64 Suppl 4:iv24–8.
Gengenbacher M, Kaufmann SH. Mycobacterium tuberculosis: success through dormancy. FEMS Microbiol Rev. 2012;36(3):514–32.
Gómez-Reino JJ, Carmona L, Valverde VR, Mola EM, Montero MD, BIOBADASER Group. Treatment of rheumatoid arthritis with tumor necrosis factor inhibitors may predispose to significant increase in tuberculosis risk: a multicenter active-surveillance report. Arthritis Rheum. 2003;48(8):2122–7.
Bruns H, Meinken C, Schauenberg P, Härter G, Kern P, Modlin RL, et al. Anti-TNF immunotherapy reduces CD8+ T-cell-mediated antimicrobial activity against Mycobacterium tuberculosis in humans. J Clin Invest. 2009;119(5):1167–77.
Saunders BM, Frank AA, Orme IM, Cooper AM. Interleukin-6 induces early gamma interferon production in the infected lung but is not required for generation of specific immunity to Mycobacterium tuberculosis infection. Infect Immun. 2000;68(6):3322–6.
Roach DR, Bean AG, Demangel C, France MP, Briscoe H, Britton WJ. TNF regulates chemokine induction essential for cell recruitment, granuloma formation, and clearance of mycobacterial infection. J Immunol. 2002;168(9):4620–7.
Rottman M, Catherinot E, Hochedez P, Emile JF, Casanova JL, Gaillard JL, et al. Importance of T cells, gamma interferon, and tumor necrosis factor in immune control of the rapid grower Mycobacterium abscessus in C57BL/6 mice. Infect Immun. 2007;75(12):5898–907.
Jo EK, Yang CS, Choi CH, Harding CV. Intracellular signalling cascades regulating innate immune responses to mycobacteria: branching out from Toll-like receptors. Cell Microbiol. 2007;9(5):1087–98.
Basu J, Shin DM, Jo EK. Mycobacterial signaling through toll-like receptors. Front Cell Infect Microbiol. 2012;2:145.
Yuk JM, Ek J. Toll-like receptors and innate immunity. J Bacteriol Virol. 2011;41:225–35.
Schorey JS, Cooper AM. Macrophage signalling upon mycobacterial infection: the MAP kinases lead the way. Cell Microbiol. 2003;5(3):133–42.
Bae YS, Oh H, Rhee SG, Yoo YD. Regulation of reactive oxygen species generation in cell signaling. Mol Cells. 2011;32(6):491–509.
Brüne B, Dehne N, Grossmann N, Jung M, Namgaladze D, Schmid T, et al. Redox control of inflammation in macrophages. Antioxid Redox Signal. 2013;19(6):595–637.
Yang CS, Shin DM, Kim KH, Lee ZW, Lee CH, Park SG, et al. NADPH oxidase 2 interaction with TLR2 is required for efficient innate immune responses to mycobacteria via cathelicidin expression. J Immunol. 2009;182(6):3696–705.
Lee HM, Yuk JM, Kim KH, Jang J, Kang G, Park JB, et al. Mycobacterium abscessus activates the NLRP3 inflammasome via Dectin-1-Syk and p62/SQSTM1. Immunol Cell Biol. 2012;90(6):601–10.
Shin DM, Yang CS, Yuk JM, Lee JY, Kim KH, et al. Mycobacterium abscessus activates the macrophage innate immune response via a physical and functional interaction between TLR2 and dectin-1. Cell Microbiol. 2008;10(8):1608–21.
Lee HM, Yuk JM, Shin DM, Yang CS, Kim KK, Choi DK, et al. Apurinic/apyrimidinic endonuclease 1 is a key modulator of keratinocyte inflammatory responses. J Immunol. 2009;183(10):6839–48.
Kim TS, Lee HM, Hk Y, Park YK, Jo EK. Intracellular signaling pathways that regulate macrophage chemokine expression in response to Mycobacterium abscessus. J Bacteriol Virol. 2012;42:121–32.
Jo EK. Mycobacterial interaction with innate receptors: TLRs, C-type lectins, and NLRs. Curr Opin Infect Dis. 2008;21(3):279–86.
Shin DM, Jeon BY, Lee HM, Jin HS, Yuk JM, Song CH, et al. Mycobacterium tuberculosis regulates autophagy, inflammation, and cell death through redox-dependent signaling. PLoS Pathog. 2010;6(12):e1001230.
Roux AL, Ray A, Pawlik A, Medjahed H, Etienne G, Rottman M, et al. Overexpression of proinflammatory TLR-2-signalling lipoproteins in hypervirulent mycobacterial variants. Cell Microbiol. 2011;13(5):692–704.
Chan ED, Bai X, Kartalija M, Orme IM, Ordway DJ. Host immune response to rapidly growing mycobacteria, an emerging cause of chronic lung disease. Am J Respir Cell Mol Biol. 2010;43(4):387–93.
Simmon KE, Pounder JI, Greene JN, Walsh F, Anderson CM, Cohen S, et al. Identification of an emerging pathogen, Mycobacterium massiliense, by rpoB sequencing of clinical isolates collected in the United States. J Clin Microbiol. 2007;45(6):1978–80.
Shin SJ, Choi GE, Cho SN, Woo SY, Jeong BH, Jeon K, et al. Mycobacterial genotypes are associated with clinical manifestation and progression of lung disease caused by Mycobacterium abscessus and Mycobacterium massiliense. Clin Infect Dis. 2013;57(1):32–9.
Flynn JL, Chan J. Immunology of tuberculosis. Annu Rev Immunol. 2001;19:93–129.
Cooper AM. Cell-mediated immune responses in tuberculosis. Annu Rev Immunol. 2009;27:393–422.
Vignal C, Guérardel Y, Kremer L, Masson M, Legrand D, Mazurier J, et al. Lipomannans, but not lipoarabinomannans, purified from Mycobacterium chelonae and Mycobacterium kansasii induce TNF-alpha and IL-8 secretion by a CD14-toll-like receptor 2-dependent mechanism. J Immunol. 2003;171(4):2014–23.
Sampaio EP, Elloumi HZ, Zelazny A, Ding L, Paulson ML, Sher A, et al. Mycobacterium abscessus and M. avium trigger Toll-like receptor 2 and distinct cytokine response in human cells. Am J Respir Cell Mol Biol. 2008;39(4):431–9.
Lee HM, Shin DM, Choi DK, Lee ZW, Kim KH, Yuk JM. Innate immune responses to Mycobacterium ulcerans via toll-like receptors and dectin-1 in human keratinocytes. Cell Microbiol. 2009;11(4):678–92.
Schorey JS, Lawrence C. The pattern recognition receptor Dectin-1: from fungi to mycobacteria. Curr Drug Targets. 2008;9(2):123–9.
Reid DM, Gow NA, Brown GD. Pattern recognition: recent insights from Dectin-1. Curr Opin Immunol. 2009;21(1):30–7.
Yadav M, Schorey JS. The beta-glucan receptor dectin-1 functions together with TLR2 to mediate macrophage activation by mycobacteria. J Exp Med. 2006;108(9):3168–75.
Sim YS, Kim SY, Kim EJ, Shin SJ, Koh WJ. Impaired expression of MAPK is associated with the downregulation of TNF-α, IL-6, and IL-10 in Mycobacterium abscessus lung disease. Tuberc Respir Dis (Seoul). 2012;72(3):275–83.
Mendoza-Coronel E, Camacho-Sandoval R, Bonifaz LC, López-Vidal Y. PD-L2 induction on dendritic cells exposed to Mycobacterium avium downregulates BCG-specific T cell response. Tuberculosis (Edinb). 2011;91(1):36–46.
Bhatnagar S, Schorey JS. Elevated mitogen-activated protein kinase signalling and increased macrophage activation in cells infected with a glycopeptidolipid-deficient Mycobacterium avium. Cell Microbiol. 2006;8(1):85–96.
Pawlik A, Garnier G, Orgeur M, Tong P, Lohan A, Le Chevalier F, et al. Identification and characterization of the genetic changes responsible for the characteristic smooth-to-rough morphotype alterations of clinically persistent Mycobacterium abscessus. Mol Microbiol. 2013.
Rhoades ER, Archambault AS, Greendyke R, Hsu FF, Streeter C, Byrd TF. Mycobacterium abscessus Glycopeptidolipids mask underlying cell wall phosphatidyl-myo-inositol mannosides blocking induction of human macrophage TNF-alpha by preventing interaction with TLR2. J Immunol. 2009;183(3):1997–2007.
Catherinot E, Clarissou J, Etienne G, Ripoll F, Emile JF, Daffé M, et al. Hypervirulence of a rough variant of the Mycobacterium abscessus type strain. Infect Immun. 2007;75(2):1055–8.
Sohn H, Kim HJ, Kim JM, Jung Kwon O, Koh WJ, Shin SJ. High virulent clinical isolates of Mycobacterium abscessus from patients with the upper lobe fibrocavitary form of pulmonary disease. Microb Pathog. 2009;47(6):321–8.
