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Mycobacterium tuberculosis–Induced Cytokine and Chemokine Expression by Human Microglia and Astrocytes: Effects of Dexamethasone
Author(s) -
R. Bryan Rock,
Shuxian Hu,
Genya Gekker,
Wen S. Sheng,
Barbara May,
Vivek Kapur,
Phillip K. Peterson
Publication year - 2005
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/498165
Subject(s) - mycobacterium tuberculosis , chemokine , microglia , immunology , tuberculosis , dexamethasone , cytokine , microbiology and biotechnology , medicine , mycobacterium , virology , biology , inflammation , pathology , endocrinology
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 microglia 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.

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