Commensal bacteria signal through TLR5 and AhR to improve barrier integrity and prevent allergic responses to food.
Commensal bacteria signal through TLR5 and AhR to improve barrier integrity and prevent allergic responses to food.
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DOI:
10.1016/j.celrep.2023.113153
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发表时间:
2023-10-31
期刊:
影响因子:
8.8
通讯作者:
中科院分区:
文献类型:
--
作者:
The increasing prevalence of food allergies has been linked to reduced commensal microbial diversity. In this article, we describe two features of allergy-protective Clostridia that contribute to their beneficial effects. Some Clostridial taxa bear flagella (a ligand for TLR5) and produce indole (a ligand for the aryl hydrocarbon receptor [AhR]). Lysates and flagella from a Clostridia consortium induced interleukin-22 (IL-22) secretion from ileal explants. IL-22 production is abrogated in explants from mice in which TLR5 or MyD88 signaling is deficient either globally or conditionally in CD11c+ antigen-presenting cells. AhR signaling in RORγt+ cells is necessary for the induction of IL-22. Mice deficient in AhR in RORγt+ cells exhibit increased intestinal permeability and are more susceptible to an anaphylactic response to food. Our findings implicate TLR5 and AhR signaling in a molecular mechanism by which commensal Clostridia protect against allergic responses to food. Depletion of populations of intestinal bacteria has been associated with the increasing prevalence of food allergy. Kemter et al. show that AhR ligands and flagella from commensal Clostridia regulate intestinal barrier permeability to limit allergen access to the systemic circulation and prevent allergic responses to food.
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影响因子:
32.4
作者:
Hou, Baidong;Reizis, Boris;DeFranco, Anthony L.
通讯作者:
DeFranco, Anthony L.
DOI:
10.1084/jem.20062648
发表时间:
2007-07-09
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Caton ML;Smith-Raska MR;Reizis B
通讯作者:
Reizis B
影响因子:
4.4
作者:
He, YW;Beers, C;Bevan, MJ
通讯作者:
Bevan, MJ
影响因子:
32.4
作者:
Chun, Eunyoung;Lavoie, Sydney;Garrett, Wendy S.
通讯作者:
Garrett, Wendy S.
影响因子:
24.5
作者:
Cani PD;Possemiers S;Van de Wiele T;Guiot Y;Everard A;Rottier O;Geurts L;Naslain D;Neyrinck A;Lambert DM;Muccioli GG;Delzenne NM
通讯作者:
Delzenne NM