Rock R Bryan, Hu Shuxian, Gekker Genya, Sheng Wen S, May Barbara, Kapur Vivek, Peterson Phillip K
Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, MN 55455, USA.
J Infect Dis. 2005 Dec 15;192(12):2054-8. doi: 10.1086/498165. Epub 2005 Nov 9.
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.
尽管皮质类固醇被推荐作为结核性脑膜炎的辅助治疗药物，但其有益作用的潜在机制仍知之甚少。在本研究中，人小胶质细胞和星形胶质细胞被结核分枝杆菌H37Rv感染，在有或没有地塞米松治疗的情况下检测细胞因子和趋化因子的表达。小胶质细胞是被结核杆菌感染的主要细胞，可引发大量多种细胞因子和趋化因子的产生。地塞米松治疗显著抑制了这些介质的产生。本研究结果支持以下观点：小胶质细胞在结核病神经发病机制中起重要作用，地塞米松可能通过调节这些脑巨噬细胞产生促炎细胞因子和趋化因子来发挥作用。
