Although corticosteroids are recommended as adjunctive therapy for tuberculous meningitis, the mechanism underlying their beneficial effect is poorly understood. In this study, human microglia and astrocytes were infected with Mycobacterium tuberculosis H37Rv, and cytokine and chemokine expression was examined with and without dexamethasone treatment. Microglia were the principal cells infected by tubercle bacilli, which elicited robust amounts of several cytokines and chemokines. Treatment with dexamethasone markedly suppressed production of these mediators. The results of this study support the concept that micreglia play an important role in neuropathogenesis of tuberculosis and that dexamethasone could operate via modulation of the production of proinflammatory cytokines and chemokines by these brain macrophages.
Bibliographical noteFunding Information:
1Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, 2Division of Infectious Diseases and International Medicine, Department of Medicine, University of Minnesota Medical School, and 3Department of Microbiology, University of Minnesota, Minneapolis
Received 24 March 2005; accepted 14 July 2005; electronically published 9 November 2005. Presented in part: 42nd annual meeting of the Infectious Diseases Society of America, Boston, Massachusetts, 29 September–3 October 2004 (grant abstract 1071). Potential conflicts of interest: none reported. Financial support: National Institutes of Health (DA-04381). Reprints or correspondence: Dr. R. Bryan Rock, Division of Infectious Diseases and International Medicine, Dept. of Medicine, University of Minnesota Medical School, 420 Delaware St. SE, Minneapolis, MN 55455 (email@example.com).