Review: Pathogenesis of Helicobacter pylori infection.
DNA methylation
H pylori cell shape
VacA
cagT4SS
chemotaxis
gastric organoids
miRNA
natural transformation
oncogenesis
Journal
Helicobacter
ISSN: 1523-5378
Titre abrégé: Helicobacter
Pays: England
ID NLM: 9605411
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
entrez:
12
9
2020
pubmed:
13
9
2020
medline:
2
7
2021
Statut:
ppublish
Résumé
The original strategies developed by Helicobacter pylori to persistently colonise its host and to deregulate its cellular functions make this bacterium an outstanding model to study host-pathogen interaction and the mechanisms responsible for bacterial-induced carcinogenesis. During the last year, significant results were obtained on the role of bacterial factors essential for gastric colonisation such as spiral shape maintenance, orientation through chemotaxis and the formation of bacteria clonal population islands inside the gastric glands. Particularities of the H pylori cell surface, a structure important for immune escape, were demonstrated. New insights in the bacterial stress response revealed the importance of DNA methylation-mediated regulation. Further findings were reported on H pylori components that mediate natural transformation and mechanisms of bacterial DNA horizontal transfer which maintain a high level of H pylori genetic variability. Within-host evolution was found to be niche-specific and probably associated with physiological differences between the antral and oxyntic gastric mucosa. In addition, with the progress of CryoEM, high-resolution structures of the major virulence factors, VacA and CagT4SS, were obtained. The use of gastric organoid models fostered research revealing, preferential accumulation of bacteria at the site of injury during infection. Several studies further characterised the role of CagA in the oncogenic properties of H pylori, identifying the activation of novel CagA-dependent pathways, leading to the promotion of genetic instabilities, epithelial-to-mesenchymal transition and finally carcinogenesis. Recent studies also highlight that microRNA-mediated regulation and epigenetic modifications, through DNA methylation, are key events in the H pylori-induced tumorigenesis process.
Substances chimiques
Antigens, Bacterial
0
Bacterial Proteins
0
VacA protein, Helicobacter pylori
0
Virulence Factors
0
cagA protein, Helicobacter pylori
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12736Subventions
Organisme : Institut Pasteur
ID : Transversal Research Program (PTR 73-17), Donation of Janssen and Odyssey Reinsurance companies
Organisme : Agence Nationale de la Recherche
ID : ANR16-CE18-0026-03
Organisme : Agence Nationale de la Recherche
ID : ANR15-CE17-0015
Organisme : Fondation pour la Recherche Médicale
ID : DBF20161136767
Informations de copyright
© 2020 John Wiley & Sons Ltd.
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