The microbial origins of food allergy.
Animals
Dysbiosis
/ immunology
Fecal Microbiota Transplantation
Food Hypersensitivity
/ immunology
Gastrointestinal Microbiome
/ immunology
Humans
Immunity, Mucosal
Immunoglobulin A
/ metabolism
Immunoglobulin E
/ metabolism
Models, Immunological
Nuclear Receptor Subfamily 1, Group F, Member 3
/ metabolism
T-Lymphocytes, Regulatory
/ immunology
Food allergy
IgA
IgE
RORγt(+) Treg
dysbiosis
fecal microbiota transplantation
microbiome
microbiota
regulatory T cells
Journal
The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002
Informations de publication
Date de publication:
03 2021
03 2021
Historique:
received:
03
11
2020
revised:
18
11
2020
accepted:
11
12
2020
pubmed:
22
12
2020
medline:
23
9
2021
entrez:
21
12
2020
Statut:
ppublish
Résumé
Food allergy (FA) is a significant public health issue, propelled by its rapidly increasing prevalence. Its sharp rise into prominence has focused attention on causative environmental factors and their interplay with the immune system in disease pathogenesis. In that regard, there is now substantial evidence that alterations in the gut microbiome early in life imprint the host gut mucosal immunity and may play a critical role in precipitating FA. These changes may impact key steps in the development of the infant gut microbiome, including its shaping by maternal factors and upon the introduction of solid food (the weaning reaction). These early-life changes may have long-range effects on host immunity that manifest later in time as disease pathology. Experimental studies have shown that resetting the host intestinal immune responses by treatment with either a healthy fecal microbiota transplantation or defined commensal bacterial taxa can prevent or treat FA. The mechanisms by which these interventions suppress FA include restoration of gut immune regulatory checkpoints, notably the retinoic orphan receptor gamma T
Identifiants
pubmed: 33347905
pii: S0091-6749(20)32410-6
doi: 10.1016/j.jaci.2020.12.624
pmc: PMC8096615
mid: NIHMS1658097
pii:
doi:
Substances chimiques
Immunoglobulin A
0
Nuclear Receptor Subfamily 1, Group F, Member 3
0
Immunoglobulin E
37341-29-0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
808-813Subventions
Organisme : NIAID NIH HHS
ID : R01 AI126915
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI132843
Pays : United States
Informations de copyright
Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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