Rewiring host-microbe interactions and barrier function during gastrointestinal inflammation.
IBD
bacterial translocation
host-defense peptides
mucosal barrier defects
nutritional immunology
Journal
Gastroenterology report
ISSN: 2052-0034
Titre abrégé: Gastroenterol Rep (Oxf)
Pays: England
ID NLM: 101620508
Informations de publication
Date de publication:
Feb 2022
Feb 2022
Historique:
received:
04
12
2021
revised:
07
01
2022
accepted:
16
02
2022
entrez:
16
3
2022
pubmed:
17
3
2022
medline:
17
3
2022
Statut:
epublish
Résumé
Organismal survival depends on a well-balanced immune system and maintenance of host-microbe mutualism. The fine-tuned relationship between the gut microbiota and host immunity is constantly challenged by opportunistic bacteria testing the integrity of gastrointestinal (GI) barrier defenses. Barrier dysfunction reduces immunological tolerance towards otherwise innocuous microbes; it is a process that may instigate chronic inflammation. Paradoxically, sustained inflammation further diminishes barrier function, enabling bacterial translocation to extra-intestinal tissues. Once translocated, these bacteria stimulate systemic inflammation, thereby compromising organ function. While genetic risk alleles associate with barrier dysfunction, environmental stressors are key triggers of GI inflammation and associated breakdown in immune tolerance towards resident gut microbes. As dietary components dictate substrate availability, they also orchestrate microbiota composition and function, including migratory and pro-inflammatory potential, thus holding the capacity to fuel both GI and extra-intestinal inflammation. Additionally, Western diet consumption may weaken barrier defenses via curbed Paneth cell function and diminished host-defense peptide secretion. This review focuses on intervenable niches of host-microbe interactions and mucosal immunity with the ambition to provide a framework of plausible strategies to improve barrier function and regain tolerance in the inflamed mucosa via nutritional intervention.
Identifiants
pubmed: 35291443
doi: 10.1093/gastro/goac008
pii: goac008
pmc: PMC8915887
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
goac008Informations de copyright
© The Author(s) 2022. Published by Oxford University Press and Sixth Affiliated Hospital of Sun Yat-sen University.
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