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致病性胞内细菌对宿主脂质途径的调节

Modulation of Host Lipid Pathways by Pathogenic Intracellular Bacteria.

作者信息

Allen Paige E, Martinez Juan J

机构信息

Vector Borne Disease Laboratories, Department of Pathobiological Sciences, LSU School of Veterinary Medicine, Baton Rouge, LA 70803, USA.

出版信息

Pathogens. 2020 Jul 28;9(8):614. doi: 10.3390/pathogens9080614.

Abstract

Lipids are a broad group of molecules required for cell maintenance and homeostasis. Various intracellular pathogens have developed mechanisms of modulating and sequestering host lipid processes for a large array of functions for both bacterial and host cell survival. Among the host cell lipid functions that intracellular bacteria exploit for infection are the modulation of host plasma membrane microdomains (lipid rafts) required for efficient bacterial entry; the recruitment of specific lipids for membrane integrity of intracellular vacuoles; and the utilization of host lipid droplets for the regulation of immune responses and for energy production through fatty acid β-oxidation and oxidative phosphorylation. The majority of published studies on the utilization of these host lipid pathways during infection have focused on intracellular bacterial pathogens that reside within a vacuole during infection and, thus, have vastly different requirements for host lipid metabolites when compared to those intracellular pathogens that are released into the host cytosol upon infection. Here we summarize the mechanisms by which intracellular bacteria sequester host lipid species and compare the modulation of host lipid pathways and metabolites during host cell infection by intracellular pathogens residing in either a vacuole or within the cytosol of infected mammalian cells. This review will also highlight common and unique host pathways necessary for intracellular bacterial growth that could potentially be targeted for therapeutic intervention.

摘要

脂质是细胞维持和体内平衡所需的一大类分子。各种细胞内病原体已发展出调节和隔离宿主脂质过程的机制,以实现细菌和宿主细胞生存所需的一系列功能。细胞内细菌用于感染的宿主细胞脂质功能包括调节高效细菌进入所需的宿主质膜微区(脂筏);募集特定脂质以维持细胞内液泡的膜完整性;以及利用宿主脂滴通过脂肪酸β氧化和氧化磷酸化来调节免疫反应和产生能量。大多数已发表的关于感染期间这些宿主脂质途径利用情况的研究都集中在感染期间驻留在液泡内的细胞内细菌病原体上,因此,与那些感染后释放到宿主细胞质中的细胞内病原体相比,它们对宿主脂质代谢物的需求有很大不同。在这里,我们总结了细胞内细菌隔离宿主脂质种类的机制,并比较了感染期间驻留在液泡或感染哺乳动物细胞胞质中的细胞内病原体对宿主脂质途径和代谢物的调节。本综述还将强调细胞内细菌生长所需的常见和独特宿主途径,这些途径可能成为治疗干预的靶点。

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