Gut IgA abundance in adult life is a major determinant of resistance to dextran sodium sulfate-colitis and can compensate for the effects of inadequate maternal IgA received by neonates.
Animals
Animals, Newborn
Bacteria
/ immunology
Bacterial Load
Colitis
/ chemically induced
Colon
/ immunology
Crosses, Genetic
Dextran Sulfate
Disease Models, Animal
Fecal Microbiota Transplantation
Feces
/ microbiology
Female
Gastrointestinal Microbiome
/ immunology
Immunoglobulin A
/ immunology
Inflammation Mediators
/ immunology
Lactation
Male
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred CBA
Mice, Inbred DBA
Permeability
Pregnancy
Species Specificity
F1 mice
backcrosses
colitis
fecal microbial transplants
foster nursing
Journal
Immunology
ISSN: 1365-2567
Titre abrégé: Immunology
Pays: England
ID NLM: 0374672
Informations de publication
Date de publication:
09 2019
09 2019
Historique:
received:
08
02
2019
revised:
23
05
2019
accepted:
26
05
2019
pubmed:
20
6
2019
medline:
3
1
2020
entrez:
20
6
2019
Statut:
ppublish
Résumé
Studies with gene-deficient and gnotobiotic mice have identified many host and microbial factors that contribute to induced colitis, but information on whether specific factors determine susceptibility under more physiological conditions is lacking. Using wild-type strains that differ in their IgA response but harbor a diverse gut microbiome, we found that the IgA-high strain CBA/CaJ (CBA) is resistant to acute colitis induced with dextran sodium sulfate (DSS), unlike the IgA-low strain C57BL/6 (B6). Resistance was associated with extensive IgA-coating of fecal bacteria, lower fecal bacterial loads and greater abundance of barrier-protective transcripts in colonic tissues under homeostatic conditions. Fecal microbial transplant (FT) experiments revealed that disease induction in B6 mice was associated with a cohort of bacteria that are not targeted by IgA. However, CBA mice continued to be resistant to colitis induction following FTs from B6 mice, indicating that they are able to contain such colitogenic members. In support of a role for bacterial exclusion in resistance, oral administration of immunoglobulins decreased DSS-induced disease in B6 mice. In F
Identifiants
pubmed: 31215020
doi: 10.1111/imm.13091
pmc: PMC6700465
doi:
Substances chimiques
Immunoglobulin A
0
Inflammation Mediators
0
Dextran Sulfate
9042-14-2
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
19-34Informations de copyright
© 2019 John Wiley & Sons Ltd.
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