Cigarette smoke inhibits BAFF expression and mucosal immunoglobulin A responses in the lung during influenza virus infection

详细信息    查看全文

• 作者：Jianmiao Wang (1)
  Qinghai Li (1)
  Jungang Xie (1)
  Yongjian Xu (1)
  
  1. Department of Respiratory and Critical Care Medicine ; Tongji Hospital ; Tongji Medical College ; Huazhong University of Science and Technology ; 1095 Jiefang Road ; Wuhan ; 430030 ; China
  
• 关键词：B cell activating factor belonging to the tumor necrosis factor family (BAFF) ; Chronic obstructive pulmonary disease ; Cigarette smoking ; Immunoglobulin A ; Influenza
• 刊名：Respiratory Research
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：16
• 期：1
• 全文大小：2,142 KB
• 参考文献：1. Arcavi, L, Benowitz, NL (2004) Cigarette smoking and infection. Arch Intern Med 164: pp. 2206-16 CrossRef
  2. Sethi, S, Murphy, TF (2008) Infection in the pathogenesis and course of chronic obstructive pulmonary disease. N Engl J Med 359: pp. 2355-65 CrossRef
  3. Pilette, C, Ouadrhiri, Y, Godding, V, Vaerman, JP, Sibille, Y (2001) Lung mucosal immunity: immunoglobulin-A revisited. Eur Respir J 18: pp. 571-88 CrossRef
  4. St盲mpfli, MR, Anderson, GP (2009) How cigarette smoke skews immune responses to promote infection, lung disease and cancer. Nat Rev Immunol 9: pp. 377-84 CrossRef
  5. Feldman, C, Anderson, R (2013) Cigarette smoking and mechanisms of susceptibility to infections of the respiratory tract and other organ systems. J Infect 67: pp. 169-84 CrossRef
  6. Bengoechea, JA (2011) Secretory IgA and COPD: a new kid on the block?. Am J Respir Crit Care Med 184: pp. 285-7 CrossRef
  7. Strugnell, RA, Wijburg, OL (2010) The role of secretory antibodies in infection immunity. Nat Rev Microbiol 8: pp. 656-67 CrossRef
  8. Cerutti, A, Puga, I, Cols, M (2011) Innate control of B cell responses. Trends Immunol 32: pp. 202-11 CrossRef
  9. Litinskiy, MB, Nardelli, B, Hilbert, DM, He, B, Schaffer, A, Casali, P (2002) DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL. Nat Immunol 3: pp. 822-9 CrossRef
  10. Xu, W, Santini, PA, Matthews, AJ, Chiu, A, Plebani, A, He, B (2008) Viral double-stranded RNA triggers Ig class switching by activating upper respiratory mucosa B cells through an innate TLR3 pathway involving BAFF. J Immunol 181: pp. 276-87 CrossRef
  11. Schiemann, B, Gommerman, JL, Vora, K, Cachero, TG, Shulga-Morskaya, S, Dobles, M (2001) An essential role for BAFF in the normal development of B cells through a BCMA-independent pathway. Sci 293: pp. 2111-4 CrossRef
  12. Kalled, SL (2006) Impact of the BAFF/BR3 axis on B cell survival, germinal center maintenance and antibody production. Semin Immunol 18: pp. 290-6 CrossRef
  13. Yamada, T, Zhang, K, Yamada, A, Zhu, D, Saxon, A (2005) B lymphocyte stimulator activates p38 mitogen-activated protein kinase in human Ig class switch recombination. Am J Respir Cell Mol Biol 32: pp. 388-94 CrossRef
  14. McNamara, PS, Fonceca, AM, Howarth, D, Correia, JB, Slupsky, JR, Trinick, RE (2013) Respiratory syncytial virus infection of airway epithelial cells, in vivo and in vitro, supports pulmonary antibody responses by inducing expression of the B cell differentiation factor BAFF. Thorax 68: pp. 76-81 CrossRef
  15. Hautamaki, RD, Kobayashi, DK, Senior, RM, Shapiro, SD (1997) Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. Sci 277: pp. 2002-4 CrossRef
  16. Liu, J, Zhao, MQ, Xu, L, Ramana, CV, Declercq, W, Vandenabeele, P (2005) Requirement for tumor necrosis factor-receptor 2 in alveolar chemokine expression depends upon the form of the ligand. Am J Respir Cell Mol Biol 33: pp. 463-9 CrossRef
  17. Jungblut, M, Oeltze, K, Zehnter, I, Hasselmann, D, Bosio, A (2009) Standardized preparation of single-cell suspensions from mouse lung tissue using the gentleMACS dissociator. J Vis Exp 29: pp. 1266
  18. Takahashi, E, Kataoka, K, Fujii, K, Chida, J, Mizuno, D, Fukui, M (2010) Attenuation of inducible respiratory immune responses by oseltamivir treatment in mice infected with influenza A virus. Microbes Infect 12: pp. 778-83 CrossRef
  19. Takahashi, E, Kataoka, K, Indalao, IL, Konoha, K, Fujii, K, Chida, J (2012) Oral clarithromycin enhances airway immunoglobulin A (IgA) immunity through induction of IgA class switching recombination and B-cell-activating factor of the tumor necrosis factor family molecule on mucosal dendritic cells in mice infected with influenza A virus. J Virol 86: pp. 10924-34 CrossRef
  20. Kato, A, Truong-Tran, AQ, Scott, AL, Matsumoto, K, Schleimer, RP (2006) Airway epithelial cells produce B cell-activating factor of TNF family by an IFN-beta-dependent mechanism. J Immunol 177: pp. 7164-72 CrossRef
  21. Eddleston, J, Lee, RU, Doerner, AM, Herschbach, J, Zuraw, BL (2011) Cigarette smoke decreases innate responses of epithelial cells to rhinovirus infection. Am J Respir Cell Mol Biol 44: pp. 118-26 CrossRef
  22. Davidson, A (2010) Targeting BAFF in autoimmunity. Curr Opin Immunol 22: pp. 732-9 CrossRef
  23. Vestbo, J, Hurd, SS, Agust铆, AG, Jones, PW, Vogelmeier, C, Anzueto, A (2013) Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med 187: pp. 347-65 CrossRef
  24. Polverino, F, Baraldo, S, Bazzan, E, Agostini, S, Turato, G, Lunardi, F (2010) A novel insight into adaptive immunity in chronic obstructive pulmonary disease: B cell activating factor belonging to the tumor necrosis factor family. Am J Respir Crit Care Med 182: pp. 1011-9 CrossRef
  25. Ladjemi MZ, Lecocq M, Weynand B, Bowen H, Gould HJ, Van Snick J, et al. Increased IgA production by B-cells in COPD via lung epithelial interleukin-6 and TACI pathways. Eur Respir J. 2014; ERJ鈥?0639鈥?014: doi:10.1183/09031936.00063914
  26. Wilkinson, TM, Donaldson, GC, Johnston, SL, Openshaw, PJ, Wedzicha, JA (2006) Respiratory syncytial virus, airway inflammation, and FEV1 decline in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 173: pp. 871-6 CrossRef
  27. Tertilt, C, Joh, J, Krause, A, Chou, P, Schneeweiss, K, Crystal, RG (2009) Expression of B-cell activating factor enhances protective immunity of a vaccine against Pseudomonasaeruginosa. Infect Immun 77: pp. 3044-55 CrossRef
  28. Reed, JL, Welliver, TP, Sims, GP, McKinney, L, Velozo, L, Avendano, L (2009) Innate immune signals modulate antiviral and polyreactive antibody responses during severe respiratory syncytial virus infection. J Infect Dis 199: pp. 1128-38 CrossRef
  29. Gohy, ST, Detry, BR, Lecocq, M, Bouzin, C, Weynand, BA, Amatngalim, GD (2014) Polymeric immunoglobulin receptor down-regulation in chronic obstructive pulmonary disease. Persistence in the cultured epithelium and role of transforming growth factor-尾. Am J Respir Crit Care Med 190: pp. 509-21 CrossRef
  30. Muramatsu, M, Kinoshita, K, Fagarasan, S, Yamada, S, Shinkai, Y, Honjo, T (2000) Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 102: pp. 553-63 CrossRef
  31. Cerutti, A (2008) The regulation of IgA class switching. Nat Rev Immunol 8: pp. 421-34 CrossRef
  32. Hoffmann, RF, Zarrintan, S, Brandenburg, SM, Kol, A, Bruin, HG, Jafari, S (2013) Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir Res 14: pp. 97 CrossRef
  33. Zuo, L, He, F, Sergakis, GG, Koozehchian, MS, Stimpfl, JN, Rong, Y (2014) Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments. Am J Physiol Lung Cell Mol Physiol 307: pp. L205-18 CrossRef
  34. Kang, MJ, Lee, CG, Lee, JY, Dela Cruz, CS, Chen, ZJ, Enelow, R (2008) Cigarette smoke selectively enhances viral PAMP- and virus-induced pulmonary innate immune and remodeling responses in mice. J Clin Invest 118: pp. 2771-84
  35. Robbins, CS, Bauer, CM, Vujicic, N, Gaschler, GJ, Lichty, BD, Brown, EG (2006) Cigarette smoke impacts immune inflammatory responses to influenza in mice. Am J Respir Crit Care Med 174: pp. 1342-51 CrossRef
  36. Wortham, BW, Eppert, BL, Motz, GT, Flury, JL, Orozco-Levi, M, Hoebe, K (2012) NKG2D mediates NK cell hyperresponsiveness and influenza-induced pathologies in a mouse model of chronic obstructive pulmonary disease. J Immunol 188: pp. 4468-75 CrossRef
  37. Diana, J, Moura, IC, Vaugier, C, Gestin, A, Tissandie, E, Beaudoin, L (2013) Secretory IgA induces tolerogenic dendritic cells through SIGNR1 dampening autoimmunity in mice. J Immunol 191: pp. 2335-43 CrossRef
  38. Mkaddem, SB, Christou, I, Rossato, E, Berthelot, L, Lehuen, A, Monteiro, RC (2014) IgA, IgA receptors, and their anti-inflammatory properties. Curr Top Microbiol Immunol 382: pp. 221-35
  
• 刊物主题：Pneumology/Respiratory System;
• 出版者：BioMed Central
• ISSN：1465-9921

文摘

Background It is incompletely understood how cigarette smoke (CS) exposure affects lung mucosal immune responses during viral respiratory infections. B cell activating factor belonging to the tumor necrosis factor family (BAFF) plays an important role in the induction of secretory immunoglobulin A (S-IgA) which is the main effector of the mucosal immune system. We therefore investigated the effects of CS exposure on BAFF expression and S-IgA responses in the lung during influenza virus infection. Methods Mice were exposed to CS and/or infected with influenza virus. Bronchoalveolar lavage fluid and lung compartments were analyzed for BAFF expression, influenza-specific S-IgA level and histological changes. Lung B cells were isolated and the activation-induced cytidine deaminase (Aicda) expression was determined. BEAS-2B cells were treated with CS extract (CSE), influenza virus, interferon beta or N-acetylcysteine and BAFF expression was measured. Results CS inhibited BAFF expression in the lung, particularly after long-term exposure. BAFF and S-IgA levels were increased during influenza virus infection. Three-month CS exposure prior to influenza virus infection resulted in reduced BAFF and S-IgA levels in the lung as well as augmented pulmonary inflammation on day 7 after infection. Prior CS exposure also caused decreased Aicda expression in lung B cells during infection. Neutralization of BAFF in the lung resulted in reduced S-IgA levels during influenza virus infection. CSE inhibited virus-mediated BAFF induction in a dose-dependent manner in BEAS-2B cells, while this inhibition of BAFF by CSE was prevented by pretreatment with the antioxidant N-acetylcysteine. Conclusions Our findings indicate that CS may hinder early mucosal IgA responses in the lung during influenza virus infection through oxidative inhibition of BAFF, which might contribute to the increased incidence and severity of viral infections in smokers.