The regenerating family member 3 β instigates IL-17A-mediated neutrophil recruitment downstream of NOD1/2 signalling for controlling colonisation resistance independently of microbiota community structure.
Animals
CARD Signaling Adaptor Proteins
/ physiology
Citrobacter rodentium
Crohn Disease
/ microbiology
Disease Models, Animal
Enterobacteriaceae Infections
/ pathology
Interleukin-17
/ physiology
Intestinal Mucosa
/ pathology
Mice
Neutrophil Infiltration
/ physiology
Nod2 Signaling Adaptor Protein
/ physiology
Receptor-Interacting Protein Serine-Threonine Kinase 2
Receptor-Interacting Protein Serine-Threonine Kinases
/ physiology
Signal Transduction
Antibacterial Peptide
Barrier Function
Colonic Microflora
Interleukins
Macrophages
Journal
Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
received:
07
05
2018
revised:
08
08
2018
accepted:
29
08
2018
pubmed:
4
10
2018
medline:
28
7
2019
entrez:
4
10
2018
Statut:
ppublish
Résumé
Loss of the Crohn's disease predisposing Colonisation resistance was evaluated in wild type and mutant mice, as well as in ex-germ-free (ex-GF) mice which were colonised either with faeces from Primary infection was similarly outcompeted in ex-GF These results unveil a previously unrecognised mechanism that efficiently protects from colonisation by diarrhoeagenic bacteria early in infection.
Identifiants
pubmed: 30279238
pii: gutjnl-2018-316757
doi: 10.1136/gutjnl-2018-316757
doi:
Substances chimiques
CARD Signaling Adaptor Proteins
0
Card9 protein, mouse
0
Il17a protein, mouse
0
Interleukin-17
0
Nod2 Signaling Adaptor Protein
0
Nod2 protein, mouse
0
Receptor-Interacting Protein Serine-Threonine Kinase 2
EC 2.7.11.1
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Ripk2 protein, mouse
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
1190-1199Informations de copyright
© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: None declared.