Caspase-3-dependent phagocyte death during systemic Salmonella enterica serovar Typhimurium infection of mice
Caspase-3-dependent phagocyte death during systemic Salmonella enterica serovar Typhimurium infection of mice
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DOI：
10.1111/j.1365-2567.2008.02814.x
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发表时间：
2008-09-01
期刊：
影响因子：
6.4
通讯作者：
Mastroeni, Pietro
中科院分区：
文献类型：
--
作者：
Grant, Andrew J.;Sheppard, Mark;Mastroeni, Pietro
肠道沙门氏菌在哺乳动物组织中的生长是由于细菌不断传播到新的宿主细胞。我们之前的研究表明，感染性肠球菌是通过随机坏死爆发从宿主细胞中释放出来的，与细胞内细菌数量无关。在这里，我们报道肝吞噬细胞可以在体内经历凋亡caspase-3介导的细胞死亡，凋亡是一种罕见的事件，在严重感染的细胞中更为普遍。密度依赖性凋亡细胞死亡可能构成了细菌传播的另一种机制，作为下注对冲策略的一部分，确保了一些细菌可以生长和持续存在的保护性细胞内环境。
Growth of Salmonella enterica in mammalian tissues results from continuous spread of bacteria to new host cells. Our previous work indicated that infective S. enterica are liberated from host cells via stochastic necrotic burst independently of intracellular bacterial numbers. Here we report that liver phagocytes can undergo apoptotic caspase-3-mediated cell death in vivo, with apoptosis being a rare event, more prevalent in heavily infected cells. The density-dependent apoptotic cell death is likely to constitute an alternative mechanism of bacterial spread as part of a bet-hedging strategy, ensuring an ongoing protective intracellular environment in which some bacteria can grow and persist.