Laskay Tamás, van Zandbergen Ger, Solbach Werner
Institute of Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany.
Immunobiology. 2008;213(3-4):183-91. doi: 10.1016/j.imbio.2007.11.010. Epub 2008 Feb 8.
Polymorphonuclear neutrophil granulocytes (PMN) are primary antimicrobial effector cells of the innate immune system and serve to destroy invading pathogens. Although most ingested microorganisms are killed readily inside PMN, several obligate or facultative intracellular pathogens survive even in this hostile environment. Extension of the life span of neutrophils is a general escape mechanism of pathogens residing in PMN. However, after 2-4 days, even infected neutrophils become apoptotic and are phagocytosed by macrophages. Since microbes entering macrophages via the uptake of infected apoptotic PMN may survive and multiply in macrophages, apoptotic neutrophils can serve as "Trojan horses" for certain pathogens. Interfering with activating signaling pathways appears to be another potent mechanism by which intracellular microorganisms suppress cellular activation in neutrophils. In addition to provide a short overview of the topic, the present review aims to summarize our own findings regarding the interaction between human neutrophils and intracellular pathogens as well as regarding the disease promoting role of apoptotic cells after infection with Leishmania major.
多形核中性粒细胞（PMN）是先天性免疫系统的主要抗菌效应细胞，用于消灭入侵的病原体。尽管大多数被吞噬的微生物在PMN内很容易被杀死，但一些专性或兼性细胞内病原体即使在这种恶劣环境中也能存活。延长中性粒细胞的寿命是病原体在PMN中生存的一种常见逃逸机制。然而，2 - 4天后，即使是被感染的中性粒细胞也会发生凋亡，并被巨噬细胞吞噬。由于通过摄取受感染的凋亡PMN进入巨噬细胞的微生物可能在巨噬细胞中存活并繁殖，凋亡的中性粒细胞可以作为某些病原体的“特洛伊木马”。干扰激活信号通路似乎是细胞内微生物抑制中性粒细胞细胞激活的另一种有效机制。除了简要概述该主题外，本综述旨在总结我们自己关于人类中性粒细胞与细胞内病原体之间相互作用以及感染硕大利什曼原虫后凋亡细胞在疾病促进作用方面的研究结果。
