期刊
TUBERCULOSIS
卷 91, 期 6, 页码 587-593出版社
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.tube.2011.06.009
关键词
Pleural tuberculosis; Pericardial tuberculosis; IL-17; IL-22; Inflammation
资金
- Wellcome Trust [WT083226, 084323, 088316, 080929/Z/06/Z]
- MRC of the UK
- German Research Foundation (DFG) [SCHE1556]
- German National Respiratory Society
- European Union [Sante/2006/105-061]
- NIH [RO1-AI065653, NO1-AI70022]
- Lily and Ernst Hausmann Research Trust
- South African Medical Research Council
- National Research Foundation
- CANNeCTIN
- Clinical Infectious Diseases Research Institute (CIDRI)
- Wellcome Trust [080929/Z/06/Z] Funding Source: Wellcome Trust
- Medical Research Council [MC_U117588499] Funding Source: researchfish
- MRC [MC_U117588499] Funding Source: UKRI
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. (C) 2011 Elsevier Ltd. All rights reserved.
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