Predominance of interleukin-22 over interleukin-17 at the site of disease in human tuberculosis
dc.contributor.author | Matthews K. | |
dc.contributor.author | Wilkinson K.A. | |
dc.contributor.author | Kalsdorf B. | |
dc.contributor.author | Roberts T. | |
dc.contributor.author | Diacon A. | |
dc.contributor.author | Walzl G. | |
dc.contributor.author | Wolske J. | |
dc.contributor.author | Ntsekhe M. | |
dc.contributor.author | Syed F. | |
dc.contributor.author | Russell J. | |
dc.contributor.author | Mayosi B.M. | |
dc.contributor.author | Dawson R. | |
dc.contributor.author | Dheda K. | |
dc.contributor.author | Wilkinson R.J. | |
dc.contributor.author | Hanekom W.A. | |
dc.contributor.author | Scriba T.J. | |
dc.date.accessioned | 2011-10-13T16:59:15Z | |
dc.date.available | 2011-10-13T16:59:15Z | |
dc.date.issued | 2011-10-13 | |
dc.description.abstract | 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. © 2011 Elsevier Ltd. All rights reserved. | |
dc.description.version | Article in Press | |
dc.identifier.citation | Tuberculosis | |
dc.identifier.citation | http://www.scopus.com/inward/record.url?eid=2-s2.0-79960265824&partnerID=40&md5=754ec0e36470fffbf52150fbbc9c330d | |
dc.identifier.issn | 14729792 | |
dc.identifier.other | 10.1016/j.tube.2011.06.009 | |
dc.identifier.uri | http://hdl.handle.net/10019.1/17041 | |
dc.title | Predominance of interleukin-22 over interleukin-17 at the site of disease in human tuberculosis | |
dc.type | Article in Press |