T4SS-dependent TLR5 activation by Helicobacter pylori infection.
Animals
Bacterial Proteins
/ immunology
Biopsy
Disease Models, Animal
Female
Gastric Mucosa
/ immunology
Helicobacter Infections
/ immunology
Helicobacter pylori
/ immunology
Host-Pathogen Interactions
/ immunology
Humans
Mice
Mice, Knockout
NF-kappa B
/ metabolism
Signal Transduction
/ immunology
Toll-Like Receptor 5
/ genetics
Type IV Secretion Systems
/ immunology
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
16 12 2019
16 12 2019
Historique:
received:
09
10
2019
accepted:
07
11
2019
entrez:
18
12
2019
pubmed:
18
12
2019
medline:
3
4
2020
Statut:
epublish
Résumé
Toll-like receptor TLR5 recognizes a conserved domain, termed D1, that is present in flagellins of several pathogenic bacteria but not in Helicobacter pylori. Highly virulent H. pylori strains possess a type IV secretion system (T4SS) for delivery of virulence factors into gastric epithelial cells. Here, we show that one of the H. pylori T4SS components, protein CagL, can act as a flagellin-independent TLR5 activator. CagL contains a D1-like motif that mediates adherence to TLR5
Identifiants
pubmed: 31844047
doi: 10.1038/s41467-019-13506-6
pii: 10.1038/s41467-019-13506-6
pmc: PMC6915727
doi:
Substances chimiques
Bacterial Proteins
0
NF-kappa B
0
TLR5 protein, human
0
Tlr5 protein, mouse
0
Toll-Like Receptor 5
0
Type IV Secretion Systems
0
cagL protein, Helicobacter pylori
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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