Molecular mechanisms of intracellular survival of M. tuberculosis inside host macrophages via regulation of caspases activation.

基于感染结核分枝杆菌（M. tuberculosis， MTB）和典型胞内细菌L. monocytogenes （LM）的宿主巨噬细胞对caspase(s)的调控，我们发现感染结核分枝杆菌（MTB）的巨噬细胞可诱导caspase-1激活，从而产生功能性炎症细胞因子IL-1β和IL-18。我们还发现MTB的毒力因子RD1参与巨噬细胞中caspase-1的激活。FasL/Fas信号通路是caspase(s)激活的重要系统。我们已经揭示了Fas信号通路参与卡介苗或LM感染小鼠IL-18的产生。

On the basis of regulation of caspase(s) in host macrophages infected with M. tuberculosis (MTB) and the typical intracellular bacteria L. monocytogenes (LM), we have shown that caspase-1 activation was induced in macrophages infected with MTB, which leads to the production of functional inflammatory cytokines IL-1β and IL-18. We also found that the virulence factor RD1 of MTB involved in the activation of caspase-1 in macrophages. FasL/Fas signaling pathway is an important systems for caspase(s) activation. We have unveiled the involvement of Fas signaling pathway for IL-18 production in mice infected with BCG or LM.