Predominance of interleukin-22 over interleukin-17 at the site of disease in human tuberculosis.

Predominance of interleukin-22 over interleukin-17 at the site of disease in human tuberculosis.
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DOI:
10.1016/j.tube.2011.06.009
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发表时间:
2011-11
期刊:
Tuberculosis (Edinburgh, Scotland)
影响因子:
--
通讯作者:
Scriba TJ
Scriba TJ
中科院分区:
其他
文献类型:
--
作者:
Matthews K;Wilkinson KA;Kalsdorf B;Roberts T;Diacon A;Walzl G;Wolske J;Ntsekhe M;Syed F;Russell J;Mayosi BM;Dawson R;Dheda K;Wilkinson RJ;Hanekom WA;Scriba TJ

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结核分枝杆菌(Mycobacterium tuberculosis,M.tb)在疾病部位的炎症反应是Th 1驱动的。Th 17细胞因子IL-17和IL-22是否有助于人类的这种反应尚不清楚。我们假设IL-17和IL-22有助于人类结核病(TB)胸膜和心包疾病部位的炎症反应。我们研究了胸腔积液和心包积液,确定结核病的网站,从艾滋病毒未感染的结核病患者。通过ELISA测量可溶性细胞因子的水平,并且通过Luminex测量MMP-9的水平。通过细胞内细胞因子染色分析支气管肺泡灌洗或心包分枝杆菌特异性T细胞细胞因子表达。IL-17在胸水或心包液中不丰富。在健康人、结核分枝杆菌感染者或结核性心包炎患者中未检测到结核分枝杆菌特异性疾病部位T细胞表达IL-17。这些数据不支持IL-17在人类已确定的TB疾病部位的主要作用。IL-22很容易检测到液体从两个疾病的网站。这些IL-22水平超过匹配的外周血水平。此外,心包液中的IL-22水平与MMP-9正相关,MMP-9是一种已知降解肺细胞外基质的酶。我们建议我们的研究结果支持IL-22在TB诱导的病理或由此产生的修复过程中的作用。
The inflammatory response to Mycobacterium tuberculosis (M.tb) at the site of disease is Th1 driven. Whether the Th17 cytokines, IL-17 and IL-22, contribute to this response in humans is unknown. We hypothesized that IL-17 and IL-22 contribute to the inflammatory response in pleural and pericardial disease sites of human tuberculosis (TB). We studied pleural and pericardial effusions, established TB disease sites, from HIV-uninfected TB patients. Levels of soluble cytokines were measured by ELISA and MMP-9 by luminex. Bronchoalveolar lavage or pericardial mycobacteria-specific T cell cytokine expression was analyzed by intracellular cytokine staining. IL-17 was not abundant in pleural or pericardial fluid. IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy, M.tb-infected persons, or patients with TB pericarditis. These data do not support a major role for IL-17 at established TB disease sites in humans. IL-22 was readily detected in fluid from both disease sites. These IL-22 levels exceeded matching peripheral blood levels. Further, IL-22 levels in pericardial fluid correlated positively with MMP-9, an enzyme known to degrade the pulmonary extracellular matrix. We propose that our findings support a role for IL-22 in TB-induced pathology or the resulting repair process.
独特的,特定的IL-17-和IL-22产生的CD4+ T细胞子集有助于人类抗细菌免疫反应。
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