Journal
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
Volume 69, Issue 1, Pages 11-19Publisher
WILEY
DOI: 10.1111/j.1365-3083.2008.02190.x
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Funding
- Department of Biotechnology
- Department of Science and Technology (DST)
- Council for Scientific and Industrial Research (CSIR), Government of India
- ICMR (Center for Advanced Study in Molecular Medicine)
- University Grants Commission
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Cyclooxygenase-2 (COX-2) is implicated in pathophysiological processes associated with the initiation or maintenance of host inflammatory responses to infection. Our results demonstrates that Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases. Further, M. bovis BCG-mediated inhibition of COX-2 or p38 mitogen-activated protein kinase could be reversed by Calyculin A, a selective inhibitor of Ser/Thr phosphatases. Moreover, M. bovis BCG inhibited the TNF-alpha-triggered NF-kappa B activation following I kappa B degradation. Taken together, these results suggest that the attenuation of COX-2 expression by vaccine strain, M. bovis BCG, represents a novel strategy to maintain robust host proinflammatory responses to subsequent challenges with virulent tuberculosis bacilli.
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