Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, WA 98195.
Program in Infectious Diseases, School of Public Health, University of California, Berkeley, Berkeley, CA 94720.
Microbiol Spectr. 2015 Dec;3(6). doi: 10.1128/microbiolspec.VMBF-0002-2014.
The coevolution of intracellular bacteria with their eukaryotic hosts has presented these pathogens with numerous challenges for their evolutionary progress and survival. Chief among these is the ability to exit from host cells, an event that is fundamentally linked to pathogen dissemination and transmission. Recent years have witnessed a major expansion of research in this area, and this chapter summarizes our current understanding of the spectrum of exit strategies that are exploited by intracellular pathogens. Clear themes regarding the mechanisms of microbial exit have emerged and are most easily conceptualized as (i) lysis of the host cell, (ii) nonlytic exit of free bacteria, and (iii) release of microorganisms into membrane-encased compartments. The adaptation of particular exit strategies is closely linked with additional themes in microbial pathogenesis, including host cell death, manipulation of host signaling pathways, and coincident activation of proinflammatory responses. This chapter will explore the molecular determinants used by intracellular pathogens to promote host cell escape and the infectious advantages each exit pathway may confer, and it will provide an evolutionary framework for the adaptation of these mechanisms.
细胞内细菌与其真核宿主的共同进化给这些病原体的进化和生存带来了诸多挑战。其中最重要的是能够从宿主细胞中逸出,这一事件与病原体的传播和传播密切相关。近年来,该领域的研究取得了重大进展,本章总结了我们目前对细胞内病原体利用的各种逸出策略的理解。关于微生物逸出机制的明确主题已经出现,并且最容易被概念化为(i)宿主细胞的裂解,(ii)游离细菌的非裂解逸出,以及(iii)微生物进入膜包裹的隔室的释放。特定逸出策略的适应与微生物发病机制中的其他主题密切相关,包括宿主细胞死亡、宿主信号通路的操纵以及伴随的促炎反应的激活。本章将探讨细胞内病原体用于促进宿主细胞逃逸的分子决定因素,以及每种逸出途径可能赋予的感染优势,并为这些机制的适应提供一个进化框架。