Vai trò quan trọng của interleukin-23 trong sự phát triển của bệnh hen suyễn do khói thuốc lá thúc đẩy

Springer Science and Business Media LLC - Tập 97 - Trang 937-949 - 2019
Hyun Seung Lee1, Da-Eun Park1, Ji-Won Lee2, Hoe-Na Kim1, Woo-Jung Song2,3, Heung-Woo Park4, Sang-Heon Cho1,4
1Institute of Allergy and Clinical Immunology, Medical Research Center, Seoul National University, Seoul, South Korea
2Division of Allergy and Clinical Immunology, Department of Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea
3Division of Allergy and Clinical Immunology, Department of Internal Medicine Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea
4Department of Internal Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea

Tóm tắt

Gần đây đã có báo cáo rằng việc tiếp xúc với khói thuốc lá trong quá trình cảm ứng dị ứng thuận lợi cho sự phát triển của bệnh hen suyễn dị ứng; tuy nhiên, các cơ chế tiềm ẩn vẫn còn chưa rõ ràng. Chúng tôi đã đánh giá vai trò của interleukin (IL-23) trong mô hình chuột hen suyễn dị ứng do chiết xuất khói thuốc lá (CSE) gây ra bằng Dermatophagoides pteronyssinus (Dp). Chuột BALB/c đã được tiếp xúc với CSE trong thời gian cảm ứng dị ứng. Kháng thể chống IL-23p19 hoặc IL-23R đã được sử dụng trong suốt thời gian cảm ứng. Chúng tôi đã đánh giá một số phản ứng miễn dịch. Sự biểu hiện của IL-23 và thụ thể IL-23 (IL-23R) đã được kiểm tra trong mô phổi. Biểu hiện IL-23 và IL-23R tăng lên trong biểu mô đường thở của chuột được cho cùng lúc Dp/CSE. Việc dùng CSE trong quá trình cảm ứng đã thúc đẩy sự cảm ứng dị ứng với Dp và sự phát triển của các triệu chứng hen suyễn. Thêm vào đó, tỉ lệ tế bào lympho bẩm sinh loại 2 (ILC2) cũng tăng lên do sự kết hợp của CSE và Dp. Việc điều trị bằng kháng thể chống IL-23 hoặc IL-23R trong quá trình cảm ứng dị ứng đã làm giảm đáng kể triệu chứng hen suyễn dị ứng và quần thể ILC2. Mức độ IL-33 và thymic stromal lymphopoietin (TSLP) cũng giảm đáng kể nhờ điều trị kháng thể chống IL-23 hoặc IL-23R. Như vậy, IL-23 có thể đóng vai trò quan trọng trong sự cảm ứng dị ứng và phát triển hen suyễn do khói thuốc lá gây ra. Về mặt lâm sàng, sự gia tăng cảm ứng dị ứng do tiếp xúc với thuốc lá gây ra khởi phát hen suyễn, và IL-23 có thể là yếu tố quan trọng trong cơ chế này.

Từ khóa

#hen suyễn dị ứng #interleukin-23 #cảm ứng dị ứng #khói thuốc lá #phản ứng miễn dịch

Tài liệu tham khảo

D’Amato G, Liccardi G, D’Amato M, Holgate S (2005) Environmental risk factors and allergic bronchial asthma. Clin Exp Allergy 35:1113–1124 Chan-Yeung M, Dimich-Ward H (2003) Respiratory health effects of exposure to environmental tobacco smoke. Respirology 8:131–139 Coultas DB (1998) Health effects of passive smoking. 8. Passive smoking and risk of adult asthma and COPD: an update. Thorax 53:381–387 Thomson NC, Chaudhuri R, Livingston E (2004) Asthma and cigarette smoking. Eur Respir J 24:822–833 Polosa R, Russo C, Caponnetto P, Bertino G, Sarva M, Antic T, Mancuso S, Al-Delaimy WK (2011) Greater severity of new onset asthma in allergic subjects who smoke: a 10-year longitudinal study. Respir Res 12:16 Comhair SA, Gaston BM, Ricci KS, Hammel J, Dweik RA, Teague WG, Meyers D, Ampleford EJ, Bleecker ER, Busse WW et al (2011) Detrimental effects of environmental tobacco smoke in relation to asthma severity. PLoS One 6:e18574 Jarvis D, Chinn S, Luczynska C, Burney P (1999) The association of smoking with sensitization to common environmental allergens: results from the European Community Respiratory Health Survey. J Allergy Clin Immunol 104:934–940 Lanckacker EA, Tournoy KG, Hammad H, Holtappels G, Lambrecht BN, Joos GF, Maes T (2013) Short cigarette smoke exposure facilitates sensitisation and asthma development in mice. Eur Respir J 41:1189–1199 Spits H, Artis D, Colonna M, Diefenbach A, Di Santo JP, Eberl G, Koyasu S, Locksley RM, McKenzie AN, Mebius RE et al (2013) Innate lymphoid cells--a proposal for uniform nomenclature. Nat Rev Immunol 13:145–149 Doherty TA (2015) At the bench: understanding group 2 innate lymphoid cells in disease. J Leukoc Biol 97:455–467 Moerloose KB, Robays LJ, Maes T, Brusselle GG, Tournoy KG, Joos GF (2006) Cigarette smoke exposure facilitates allergic sensitization in mice. Respir Res 7:49 Oppmann B, Lesley R, Blom B, Timans JC, Xu Y, Hunte B, Vega F, Yu N, Wang J, Singh K et al (2000) Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity 13:715–725 Lankford CS, Frucht DM (2003) A unique role for IL-23 in promoting cellular immunity. J Leukoc Biol 73:49–56 Kopp T, Lenz P, Bello-Fernandez C, Kastelein RA, Kupper TS, Stingl G (2003) IL-23 production by cosecretion of endogenous p19 and transgenic p40 in keratin 14/p40 transgenic mice: evidence for enhanced cutaneous immunity. J Immunol 170:5438–5444 Chan JR, Blumenschein W, Murphy E, Diveu C, Wiekowski M, Abbondanzo S, Lucian L, Geissler R, Brodie S, Kimball AB et al (2006) IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med 203:2577–2587 Zaba LC, Cardinale I, Gilleaudeau P, Sullivan-Whalen M, Suarez-Farinas M, Fuentes-Duculan J, Novitskaya I, Khatcherian A, Bluth MJ, Lowes MA et al (2007) Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses. J Exp Med 204:3183–3194 Piskin G, Tursen U, Sylva-Steenland RM, Bos JD, Teunissen MB (2004) Clinical improvement in chronic plaque-type psoriasis lesions after narrow-band UVB therapy is accompanied by a decrease in the expression of IFN-gamma inducers -- IL-12, IL-18 and IL-23. Exp Dermatol 13:764–772 Peng J, Yang XO, Chang SH, Yang J, Dong C (2010) IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation. Cell Res 20:62–71 Wakashin H, Hirose K, Maezawa Y, Kagami S, Suto A, Watanabe N, Saito Y, Hatano M, Tokuhisa T, Iwakura Y et al (2008) IL-23 and Th17 cells enhance Th2-cell-mediated eosinophilic airway inflammation in mice. Am J Respir Crit Care Med 178:1023–1032 Lee HS, Park HW, Song WJ, Jeon EY, Bang B, Shim EJ, Moon HG, Kim YK, Kang HR, Min KU et al (2016) TNF-alpha enhance Th2 and Th17 immune responses regulating by IL23 during sensitization in asthma model. Cytokine 79:23–30 Lee HS, Park DE, Lee JW, Chang Y, Kim HY, Song WJ, Kang HR, Park HW, Chang YS, Cho SH (2017) IL-23 secreted by bronchial epithelial cells contributes to allergic sensitization in asthma model: role of IL-23 secreted by bronchial epithelial cells. Am J Physiol Lung Cell Mol Physiol 312:L13–L21 Cornelissen F, Asmawidjaja PS, Mus AM, Corneth O, Kikly K, Lubberts E (2013) IL-23 dependent and independent stages of experimental arthritis: no clinical effect of therapeutic IL-23p19 inhibition in collagen-induced arthritis. PLoS One 8:e57553 Sawa S, Lochner M, Satoh-Takayama N, Dulauroy S, Berard M, Kleinschek M, Cua D, Di Santo JP, Eberl G (2011) RORγt+ innate lymphoid cells regulate intestinal homeostasis by integrating negative signals from the symbiotic microbiota. Nat Immunol 12:320–326 Bartemes KR, Iijima K, Kobayashi T, Kephart GM, McKenzie AN, Kita H (2012) IL-33-responsive lineage- CD25+ CD44(hi) lymphoid cells mediate innate type 2 immunity and allergic inflammation in the lungs. J Immunol 188:1503–1513 Halim TY, Krauss RH, Sun AC, Takei F (2012) Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation. Immunity 36:451–463 Martinez-Gonzalez I, Steer CA, Takei F (2015) Lung ILC2s link innate and adaptive responses in allergic inflammation. Trends Immunol 36:189–195 Parham C, Chirica M, Timans J, Vaisberg E, Travis M, Cheung J, Pflanz S, Zhang R, Singh KP, Vega F et al (2002) A receptor for the heterodimeric cytokine IL-23 is composed of IL-12Rbeta1 and a novel cytokine receptor subunit, IL-23R. J Immunol 168:5699–5708 McKenzie AN (2014) Type-2 innate lymphoid cells in asthma and allergy. Ann Am Thorac Soc 11(Suppl 5):S263–S270 Jia Y, Fang X, Zhu X, Bai C, Zhu L, Jin M, Wang X, Hu M, Tang R, Chen Z (2016) IL-13(+) type 2 innate lymphoid cells correlate with asthma control status and treatment response. Am J Respir Cell Mol Biol 55:675–683 Abraham C, Cho JH (2009) IL-23 and autoimmunity: new insights into the pathogenesis of inflammatory bowel disease. Annu Rev Med 60:97–110 Di Cesare A, Di Meglio P, Nestle FO (2009) The IL-23/Th17 axis in the immunopathogenesis of psoriasis. J Investig Dermatol 129:1339–1350 Cargill M, Schrodi SJ, Chang M, Garcia VE, Brandon R, Callis KP, Matsunami N, Ardlie KG, Civello D, Catanese JJ et al (2007) A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet 80:273–290 Maldonado-Lopez R, Moser M (2001) Dendritic cell subsets and the regulation of Th1/Th2 responses. Semin Immunol 13:275–282 Cates EC, Fattouh R, Wattie J, Inman MD, Goncharova S, Coyle AJ, Gutierrez-Ramos JC, Jordana M (2004) Intranasal exposure of mice to house dust mite elicits allergic airway inflammation via a GM-CSF-mediated mechanism. J Immunol 173:6384–6392 Halim TYF, McKenzie ANJ (2013) New kids on the block: group 2 innate lymphoid cells and type 2 inflammation in the lung. Chest 144:1681–1686 Cua DJ, Sherlock J, Chen Y, Murphy CA, Joyce B, Seymour B, Lucian L, To W, Kwan S, Churakova T et al (2003) Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature 421:744–748 McKenzie ANJ, Spits H, Eberl G (2014) Innate lymphoid cells in inflammation and immunity. Immunity 41:366–374 Huang GO, Belfort MA, Whitehead WE, Olutoye OO, Castillo J, Castillo H, Ostermaier KK, Koh CJ, Tu DD (2017) Early postnatal bladder function in fetoscopic myelomeningocele repair patients. J Pediatr Rehabil Med 10:327–333 Kumar S, Lanckacker E, Dentener M, Bracke K, Provoost S, De Grove K, Brusselle G, Wouters E, Maes T, Joos G (2016) Aggravation of allergic airway inflammation by cigarette smoke in mice is CD44-dependent. PLoS One 11:e0151113 Elliott MK, Sisson JH, West WW, Wyatt TA (2006) Differential in vivo effects of whole cigarette smoke exposure versus cigarette smoke extract on mouse ciliated tracheal epithelium. Exp Lung Res 32:99–118 Nakamura Y, Miyata M, Ohba T, Ando T, Hatsushika K, Suenaga F, Shimokawa N, Ohnuma Y, Katoh R, Ogawa H et al (2008) Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to T(H)2-type immune responses and airway inflammation. J Allergy Clin Immunol 122:1208–1214 Trimble NJ, Botelho FM, Bauer CM, Fattouh R, Stampfli MR (2009) Adjuvant and anti-inflammatory properties of cigarette smoke in murine allergic airway inflammation. Am J Respir Cell Mol Biol 40:38–46 Botelho FM, Llop-Guevara A, Trimble NJ, Nikota JK, Bauer CM, Lambert KN, Kianpour S, Jordana M, Stampfli MR (2011) Cigarette smoke differentially affects eosinophilia and remodeling in a model of house dust mite asthma. Am J Respir Cell Mol Biol 45:753–760 Alyasin S, Amin R, Fazel A, Karimi MH, Nabavizadeh SH, Esmaeilzadeh H, Babaei M (2017) IL-23 gene and protein expression in childhood asthma. Iranian J Immunol 14:73–80 Abdollahi E, Tavasolian F, Momtazi-Borojeni AA, Samadi M, Rafatpanah H (2016) Protective role of R381Q (rs11209026) polymorphism in IL-23R gene in immune-mediated diseases: a comprehensive review. J Immunotoxicol 13:286–300 Kim HY, Shin YH, Han MY (2014) Determinants of sensitization to allergen in infants and young children. Korean J Pediatr 57:205–210 Gold MJ, Antignano F, Halim TY, Hirota JA, Blanchet MR, Zaph C, Takei F, McNagny KM (2014) Group 2 innate lymphoid cells facilitate sensitization to local, but not systemic, TH2-inducing allergen exposures. J Allergy Clin Immunol 133:1142–1148 Licona-Limon P, Kim LK, Palm NW, Flavell RA (2013) TH2, allergy and group 2 innate lymphoid cells. Nat Immunol 14:536–542