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MCOLN1/TRPML1 抑制——是 逃避自噬杀伤和抗生素清除治疗的一种新策略。

MCOLN1/TRPML1 inhibition - a novel strategy used by to escape autophagic killing and antibiotic eradication therapy .

机构信息

Cell Biology Program.

Division of Gastroenterology, Hepatology and Nutrition, The Hospital for Sick Children, Toronto, ON, Canada.

出版信息

Autophagy. 2020 Jan;16(1):169-170. doi: 10.1080/15548627.2019.1677322. Epub 2019 Oct 13.

DOI:10.1080/15548627.2019.1677322
PMID:31599196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6984606/
Abstract

Inhibition of host macroautophagy/autophagy is one of the strategies used by several intracellular pathogens, including , to escape killing. Here we discuss our recent work that revealed the novel mechanism by which the vacuolating cytotoxin A (VacA) produced by inhibits lysosomal and autophagic killing. We discovered that VacA impairs the activity of the lysosomal calcium channel MCOLN1/TRPML1 leading to the formation of enlarged, dysfunctional lysosomes and autophagosomes that serve as an intracellular niche, which allows the bacteria to escape eradication therapy.

摘要

宿主巨自噬/自噬的抑制是包括 在内的几种细胞内病原体用来逃避杀伤的策略之一。在这里，我们讨论了我们最近的工作，揭示了由 产生的空泡细胞毒素 A (VacA) 抑制溶酶体和自噬杀伤的新机制。我们发现 VacA 损害溶酶体钙通道 MCOLN1/TRPML1 的活性，导致形成扩大的、功能失调的溶酶体和自噬体，作为一个细胞内小生境，使细菌能够逃避清除治疗。

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本文引用的文献

1
VacA generates a protective intracellular reservoir for Helicobacter pylori that is eliminated by activation of the lysosomal calcium channel TRPML1.空泡毒素 VacA 为幽门螺杆菌生成保护性的细胞内储库，该储库可通过溶酶体钙通道 TRPML1 的激活而被清除。
Nat Microbiol. 2019 Aug;4(8):1411-1423. doi: 10.1038/s41564-019-0441-6. Epub 2019 May 20.