Consequences of Metabolic Interactions during Staphylococcus aureus Infection.

Consequences of Metabolic Interactions during Staphylococcus aureus Infection.
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DOI:
10.3390/toxins12090581
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发表时间:
2020-09-09
期刊:
影响因子:
4.2
通讯作者:
Wong Fok Lung T
Wong Fok Lung T
中科院分区:
医学2区
文献类型:
--
作者:
Prince A;Wong Fok Lung T

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金黄色葡萄球菌是一种代谢灵活的病原体,会在不同的环境中引起感染。一系列的毒力因子,包括分泌的毒素,使金黄色葡萄球菌能够在不同的环境中定居,并通过几个离散的途径中的任何一个开始感染。在这些感染期间,金黄色葡萄球菌和宿主细胞都会相互竞争营养物质,并重新调整自己的新陈代谢以求生存。这种代谢相互作用/串扰决定了感染的结果。宿主免疫细胞代谢途径的重新编程不仅产生三磷酸腺苷(ATP)以满足感染过程中细胞的能量需求,而且还激活最终细菌清除的抗菌反应,包括细胞死亡途径。宿主免疫细胞施加的选择压力导致适应慢性化的细菌突变体的出现。这些寄主适应突变体的特征通常是其自身代谢基因的表达发生实质性变化,或者涉及代谢和生物膜形成的基因发生突变。宿主适应的金黄色葡萄球菌可以通过几种机制重新连接免疫细胞或从免疫细胞的代谢活动中受益,从而导致持续感染。在这篇综述中,我们讨论了金黄色葡萄球菌如何激活宿主的先天性免疫信号,从而导致免疫代谢压力,从而塑造金黄色葡萄球菌的代谢适应,并决定感染的结局。
Staphylococcus aureus is a metabolically flexible pathogen that causes infection in diverse settings. An array of virulence factors, including the secreted toxins, enables S. aureus to colonize different environmental niches and initiate infections by any of several discrete pathways. During these infections, both S. aureus and host cells compete with each other for nutrients and remodel their metabolism for survival. This metabolic interaction/crosstalk determines the outcome of the infection. The reprogramming of metabolic pathways in host immune cells not only generates adenosine triphosphate (ATP) to meet the cellular energy requirements during the infection process but also activates antimicrobial responses for eventual bacterial clearance, including cell death pathways. The selective pressure exerted by host immune cells leads to the emergence of bacterial mutants adapted for chronicity. These host-adapted mutants are often characterized by substantial changes in the expression of their own metabolic genes, or by mutations in genes involved in metabolism and biofilm formation. Host-adapted S. aureus can rewire or benefit from the metabolic activities of the immune cells via several mechanisms to cause persistent infection. In this review, we discuss how S. aureus activates host innate immune signaling, which results in an immune metabolic pressure that shapes S. aureus metabolic adaptation and determines the outcome of the infection.
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