A specific gene-microbe interaction drives the development of Crohn's disease-like colitis in mice.
Animals
Bacteria
/ immunology
Crohn Disease
/ genetics
Disease Models, Animal
Dysbiosis
/ genetics
Female
Host Microbial Interactions
/ genetics
Immunity, Innate
/ genetics
Immunoglobulins
/ immunology
Intestinal Mucosa
/ immunology
Male
Mice
Mice, Knockout
NADPH Oxidase 2
/ genetics
Neutrophil Infiltration
Neutrophils
/ immunology
Nod2 Signaling Adaptor Protein
/ genetics
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
19 04 2019
19 04 2019
Historique:
received:
19
12
2018
accepted:
07
03
2019
entrez:
21
4
2019
pubmed:
21
4
2019
medline:
3
4
2020
Statut:
ppublish
Résumé
Bacterial dysbiosis is associated with Crohn's disease (CD), a chronic intestinal inflammatory disorder thought to result from an abnormal immune response against intestinal bacteria in genetically susceptible individuals. However, it is unclear whether dysbiosis is a cause or consequence of intestinal inflammation and whether overall dysbiosis or specific bacteria trigger the disease. Here, we show that the combined deficiency of NOD2 and phagocyte NADPH oxidase, two CD susceptibility genes, triggers early-onset spontaneous T
Identifiants
pubmed: 31004013
pii: 4/34/eaaw4341
doi: 10.1126/sciimmunol.aaw4341
pmc: PMC8882361
mid: NIHMS1717589
pii:
doi:
Substances chimiques
Immunoglobulins
0
Nod2 Signaling Adaptor Protein
0
Nod2 protein, mouse
0
Cybb protein, mouse
EC 1.6.3.-
NADPH Oxidase 2
EC 1.6.3.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK034933
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK061707
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK091191
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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