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

Matthews K. ; Wilkinson K.A. ; Kalsdorf B. ; Roberts T. ; Diacon A. ; Walzl G. ; Wolske J. ; Ntsekhe M. ; Syed F. ; Russell J. ; Mayosi B.M. ; Dawson R. ; Dheda K. ; Wilkinson R.J. ; Hanekom W.A. ; Scriba T.J. (2011-10-13)

Article in Press

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.

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