About: Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate

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About: Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate
Creator	Chen, Yu-An Chen, Yu-Lun Lai, Chih-Ho Wang, Wen-Ching Sit, Wei
source	Elsevier; Medline; PMC
abstract	Abstract Helicobacter pylori colonizes human stomach mucosa and its infection causes gastrointestinal diseases with variable severity. Bacterial infection stimulates autophagy, which is a part of innate immunity used to eliminate intracellular pathogens. Several intracellular bacteria have evolved multipronged strategies to circumvent this conserved system and thereby enhance their chance of intracellular survival. Nonetheless, studies on H. pylori have produced inconsistent results, showing either elevated or reduced clearance efficiency of intracellular bacteria through autophagy. In this review, we summarize recent studies on the mechanisms involved in autophagy induced by H. pylori and the fate of intracellular bacteria.
has issue date	2020-02-04(xsd:dateTime)
bibo:doi	10.1016/j.semcdb.2020.01.007
bibo:pmid	32033828
has license	els-covid
sha1sum (hex)	1b80c0f06f566e0741e678da7847b7443ead9317
schema:url	https://doi.org/10.1016/j.semcdb.2020.01.007
resource representing a document's title	Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate
has PubMed Central identifier	PMC7102552
has PubMed identifier	32033828
schema:publication	Semin Cell Dev Biol
resource representing a document's body	covid:1b80c0f06f566e0741e678da7847b7443ead9317#body_text
is schema:about of	named entity 'conserved' named entity 'studies' named entity 'autophagy' named entity 'mechanisms' named entity 'ITS' »more»

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