期刊文献+

IL-17在沙眼衣原体呼吸道感染中的早期表达及其与机体防御关系 被引量:1

The Early IL-17 Expression in Chlamydia Trachomatis Respiratory Infection and Its Relationship with Immune Defence
下载PDF
导出
摘要 目的:探讨炎症性细胞因子IL-17在沙眼衣原体呼吸道感染中的早期表达及与机体防御的关系。方法:用沙眼衣原体小鼠肺炎株(MoPn)通过鼻腔感染小鼠,用IFA检测衣原体在肺组织的生长;通过ELISA检测小鼠肺组织IL-17、IL-6、IL-8、TNF-α、IL-1α和IL-1β等炎症性细胞因子表达。结果:MoPn感染后第1天,肺组织有衣原体生长,于感染后第8天达高峰;感染后第2天,IL-17在小鼠肺组织中的表达达峰值,并很快下降;TNFα、IL-1α、IL-1β和IL-6在感染后第3天达到峰值,而IL-8则在第8天出现高峰。结论:IL-17在衣原体肺炎早期出现,能提高局部IL-6,IL-8,TNF-α,IL-1α,IL-1β的表达。这些结果显示IL-17早期表达可能作为固有免疫反应成分在起动宿主抵御细胞内病原体感染中发挥重要的作用。 Objective:To evaluate the early Il-17 expression in Chlamydia trachornatis respiratory infection and its relationship with immune defence. Methods: A murine model of pneumonia induced by intranasal inoculation with Chlarnydia trachomatis mouse pneumonitis(MoPn, now classified as a new species C. muridarurn) biovar was used for the study. Chlamydial growth in the lung was assessed by inoculating HeLa cell monolayer with lung homogenates followed by IFA. IL-17 and other cytokines such as TNFa, IL-6, IL-8, IL-laand IL-1βwere measured by ELISA. Results:Chlamydial growth in the lung was found on the lst day after infection,and reached its peak on the 8th day with subsequent decline in quantity. IL-17 peaked at 48h while other cytokines peaked on the 3rd day(e, g. TNFa, 1L-6, IL-lttand IL-lβ) or later (IL-8). Conclusion: II.-17 is pro- duced early in airway upon Chlamydia trachomatis, it can enhance high production of TNFa, IL-6, IL-8, IL- laand IL-lβ in the lung. These suggest that an early IL-17 response as art innate immunity component should play an important role in initiating host defense against infection with Chlamydia trackornatis in the airway.
出处 《河北北方学院学报(医学版)》 2009年第4期7-10,共4页 Journal of Hebei North University:Medical Edition
基金 US National Institute of Health基金资助
关键词 衣原体/沙眼 IL-17 呼吸道感染 小鼠 Chlamydia Trachomatis, 1L-17, Respiratory Tract Infections, Mice
  • 相关文献

参考文献18

  • 1Morrison RP,Caldwell HD. Immunity to murine chlamydial genital infeetion[J]. Infecl Immun,2002,70(6) :2741 -2751.
  • 2Morrison SG, Morrison RP. A predominant role for antibody in acquired immunity to chlamydial genital tract reinfection[J]. J Immunol,2005,175(11) :7536 -7542.
  • 3Kimura A,Naka T,Kishimoto T. IL-6 -dependent and- independent pathways in the development of interleukin 17 producing T helper cells[J]. Proc Natl Acad Sci USA, 2007, 104(29):12099 -12104.
  • 4Rouvier E, Luciani MF, Mattei MG, ct al. CTLA-8, cloned from an activated T cell, bearing AU-rich messenger RNA instabilily sequences, and homologous to a herpesvirus saimiri gene[J]. J Immunol,1993,150(12) :5445 -5456.
  • 5Chabaud M, Fossiez F, Taupin JL, et al. Enhancing effects of IL-17 on IL-1-induced IL-6 and leukemia inhibitory factor production by rheumatoid arthr tis synoviocytes and its regulation by Th2 cytokines[J]. J Immunol, 1998,161 ( 1 ) : 409- 414.
  • 6Jovanovic DV, Battista JA, Martel P J, et al. IL-17 stimulates the production and expression of proinflammatory cytokines,IL-1h and TNF-a by human macrophages[J]. J Immunol, 1998,160(7) : 3513-3521.
  • 7Andoh A,Fujino S,Bamba S,el al. IL-17 selectively down- regulates TNF-a-induced RANTES gene expression in human colonic subepithelial myofibrobIasts[J]. J Immunol, 2002,169(4) :1683- 1687.
  • 8Maertzdorf J, Osterhaus AD, Verjans GM. IL-17 expression in human herpetic stromal keratitis: modulatory effects on chemokine production by corneal fibroblasts[J]. J Immunol, 2002,169 (10) : 5897-5903.
  • 9Langrish CL,Chen Y,Blumenschein WM,et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation[J].J Exp Med,2005,201(2) :233-240.
  • 10Yen D,Cheung J,Scheerens H,et al. IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6[J].J Clin Invest,2006,116(5):1310-1316.

同被引文献21

  • 1Moore-Connors JM, Fraser R, Halperin SA, et al. CD4(+)CD25 (+) Foxp3 (+) regulatory T cells promote Thl7 responses and gen- ital tract inflammation upon intraeellular Chlamydia muridarum in- fection[J]. J Immunol, 2013,191(6) : 3430-3439.
  • 2Park H, Li Z, Yang XO,et al. A distinct lineage of CIM T cells regulates tissue inflammation by producing interleukin 17[ JJ. Nat Immunol, 2005, 6(11) : 1133-1141.
  • 3Moseley TA, Haudenschild DR, Rose L, et al. Interleukin-17 family and IL-17 receptors [J]. Cytokine Growth Factor Rev, 2003,14(2) : 155-174.
  • 4Matsuzaki G, Umemura M. lnterleukin-17 as an effector molecule of innate and acquired immunity against infections [ J]. Microbiel Immunol, 2007,51 (12) : 1139-1147.
  • 5Harris TJ, Grosso JF, Yen HR,et al. Cutting edge: An in vivo re- quirement for STAT3 signaling in TH17 development and TH17- dependent autoimmunity [ J ]. J Immunol, 2007,179 ( 7 ) : 4313- 4317.
  • 6Stumhofer JS, Laurence A, Wilson EH,et al. Interleukin 27 nega- tively regulates the development of interleukin 17-producing T helper cells during chronic inflammation of the central nervous sys- tem [ J ]. Nat Immuno1,2006,7 (9) : 937-945.
  • 7Nakamura R, Shibata K, Yamada H, et al. Tyk2-signaling plays an important role in host defense against Escherichia coli through IL-23-induced IL-17 production by gammadelta T cells[J]. J Im- mnnol, 2008, 181(3): 2071-2075.
  • 8Michel ML, Keller AC, Paget C ,et al. Identification of an IL-17- producing NK1.1 (neg) iNKT cell population involved in airway neutrophilia[ J 1. J Exp Med, 2007, 204 ( 5 ) : 995-1001.
  • 9Potzl J, Botteron C, Tausch E,et al. Tracing functional antigen- specific CCR6 Thl7 cells after vaccination [ J ]. PLoS One, 2008, 3(8) : e2951.
  • 10Torchinsky MB, Garaude J, Martin AP, et al . Innate immune recognition of infected apoptotic cells directs T(H) 17 cell differ- entiation[J]. Nature,2009, 458(7234): 78-82.

引证文献1

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部