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棘阿米巴原虫对嗜肺军团菌感染反应的蛋白质组学分析。

Proteomic analysis of Acanthamoeba castellanii response to Legionella pneumophila infection.

机构信息

Ecologie et Biologie des Interactions, UMR CNRS 7267, Université de Poitiers, 86073 Poitiers, France.

出版信息

FEMS Microbiol Lett. 2023 Jan 17;370. doi: 10.1093/femsle/fnad086.

DOI:10.1093/femsle/fnad086
PMID:37653467
Abstract

Legionella pneumophila is an opportunistic pathogen responsible for Legionnaires' disease or Legionellosis. This bacterium is found in the environment interacting with free-living amoebae such as Acanthamoeba castellanii. Until now, proteomic analyses have been done in amoebae infected with L. pneumophila but focused on the Legionella-containing vacuole. In this study, we propose a global proteomic analysis of the A. castellanii proteome following infection with L. pneumophila wild-type (WT) or with an isogenic ΔdotA mutant strain, which is unable to replicate intracellularly. We found that infection with L. pneumophila WT leads to reduced levels of A. castellanii proteins associated with lipid homeostasis/metabolism, GTPase regulation, and kinase. The levels of organelle-associated proteins were also decreased during infection. Legionellapneumophila WT infection leads to increased levels of proteins associated with polyubiquitination, folding or degradation, and antioxidant activities. This study reinforces our knowledge of this too little explored but so fundamental interaction between L. pneumophila and A. castellanii, to understand how the bacterium could resist amoeba digestion.

摘要

嗜肺军团菌是一种机会性病原体,可导致军团病或军团菌病。这种细菌存在于环境中,与自由生活的变形虫(如棘阿米巴)相互作用。到目前为止,已经对感染嗜肺军团菌的变形虫进行了蛋白质组学分析,但主要集中在包含军团菌的空泡上。在这项研究中,我们提出了对感染野生型(WT)嗜肺军团菌或不能在细胞内复制的同源缺失Δ dotA 突变株的棘阿米巴的全蛋白质组学分析。我们发现,感染嗜肺军团菌 WT 导致与脂质动态平衡/代谢、GTPase 调节和激酶相关的棘阿米巴蛋白水平降低。在感染过程中,细胞器相关蛋白的水平也降低了。嗜肺军团菌 WT 感染导致与多泛素化、折叠或降解以及抗氧化活性相关的蛋白水平增加。这项研究加强了我们对嗜肺军团菌和棘阿米巴之间这种研究较少但非常基础的相互作用的认识,以了解细菌如何抵抗阿米巴的消化。

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Proteomic analysis of Acanthamoeba castellanii response to Legionella pneumophila infection.棘阿米巴原虫对嗜肺军团菌感染反应的蛋白质组学分析。
FEMS Microbiol Lett. 2023 Jan 17;370. doi: 10.1093/femsle/fnad086.
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