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钙对细菌毒力的调节作用。

Calcium Regulation of Bacterial Virulence.

机构信息

Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater, OK, USA.

Department of Microbiology and Center for Biofilm Engineering, Montana State University, Bozeman, MT, USA.

出版信息

Adv Exp Med Biol. 2020;1131:827-855. doi: 10.1007/978-3-030-12457-1_33.

Abstract

Calcium (Ca) is a universal signaling ion, whose major informational role shaped the evolution of signaling pathways, enabling cellular communications and responsiveness to both the intracellular and extracellular environments. Elaborate Ca regulatory networks have been well characterized in eukaryotic cells, where Ca regulates a number of essential cellular processes, ranging from cell division, transport and motility, to apoptosis and pathogenesis. However, in bacteria, the knowledge on Ca signaling is still fragmentary. This is complicated by the large variability of environments that bacteria inhabit with diverse levels of Ca. Yet another complication arises when bacterial pathogens invade a host and become exposed to different levels of Ca that (1) are tightly regulated by the host, (2) control host defenses including immune responses to bacterial infections, and (3) become impaired during diseases. The invading pathogens evolved to recognize and respond to the host Ca, triggering the molecular mechanisms of adhesion, biofilm formation, host cellular damage, and host-defense resistance, processes enabling the development of persistent infections. In this review, we discuss: (1) Ca as a determinant of a host environment for invading bacterial pathogens, (2) the role of Ca in regulating main events of host colonization and bacterial virulence, and (3) the molecular mechanisms of Ca signaling in bacterial pathogens.

摘要

钙(Ca)是一种普遍的信号离子,其主要的信息作用塑造了信号通路的进化,使细胞能够对细胞内和细胞外环境进行通讯和响应。在真核细胞中,已经很好地描述了精细的 Ca 调节网络,Ca 调节着许多基本的细胞过程,从细胞分裂、运输和运动到细胞凋亡和发病机制。然而,在细菌中,Ca 信号的知识仍然很零散。这是由于细菌栖息的环境变化很大,Ca 水平也各不相同。当细菌病原体侵入宿主并暴露于不同水平的 Ca 时,又出现了另一个复杂情况:(1) Ca 由宿主严格调控;(2) 控制宿主防御,包括对细菌感染的免疫反应;(3) 在疾病期间受损。入侵病原体进化为识别和响应宿主 Ca,引发粘附、生物膜形成、宿主细胞损伤和宿主防御抵抗的分子机制,这些过程使持续性感染得以发展。在这篇综述中,我们讨论了:(1) Ca 作为入侵细菌病原体宿主环境的决定因素;(2) Ca 在调节宿主定植和细菌毒力的主要事件中的作用;(3) Ca 信号在细菌病原体中的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e355/7473484/f763d43f471f/nihms-1623354-f0001.jpg

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