Navarre W W, Zychlinsky A
Skirball Institute for Biomolecular Medicine, Department of Microbiology and Kaplan Cancer Center, New York University School of Medicine, NY 10028, USA.
Cell Microbiol. 2000 Aug;2(4):265-73. doi: 10.1046/j.1462-5822.2000.00056.x.
Microbe-macrophage interactions play a central role in the pathogenesis of many infections. Several bacterial pathogens induce apoptosis specifically in macrophages, but the mechanisms by which it occurs differ, and the resulting pathology can take different courses. Macrophage death caused by Shigella flexneri and Salmonella spp. has been shown to result in the release of pro-inflammatory cytokines. Conversely, Yersinia spp. induce apoptosis by suppressing the signalling pathways that lead to the production of tumour necrosis factor (TNF)-alpha, a cytokine essential for the control of this infection. It is likely that there are a variety of reasons why macrophages are particularly susceptible to pathogen-induced apoptosis. One reason may be the expression of surface receptors that recognize highly conserved bacterial components, such as lipopolysaccharide (LPS) and bacterial lipoproteins (BLPs). These receptors have recently been shown to activate pro-apoptotic signalling pathways. The roles of macrophage apoptosis in different disease processes are discussed.
微生物与巨噬细胞的相互作用在许多感染的发病机制中起着核心作用。几种细菌病原体可特异性诱导巨噬细胞凋亡,但其发生机制各不相同,所导致的病理过程也可能不同。弗氏志贺菌和沙门氏菌属引起的巨噬细胞死亡已被证明会导致促炎细胞因子的释放。相反,耶尔森菌属通过抑制导致肿瘤坏死因子(TNF)-α产生的信号通路来诱导凋亡,TNF-α是控制这种感染所必需的一种细胞因子。巨噬细胞特别容易受到病原体诱导的凋亡影响,原因可能多种多样。一个原因可能是识别高度保守细菌成分的表面受体的表达,如脂多糖(LPS)和细菌脂蛋白(BLP)。最近已证明这些受体可激活促凋亡信号通路。本文讨论了巨噬细胞凋亡在不同疾病过程中的作用。