Gut Microbial Metabolites Induce Donor-Specific Tolerance of Kidney Allografts through Induction of T Regulatory Cells by Short-Chain Fatty Acids.


Journal

Journal of the American Society of Nephrology : JASN
ISSN: 1533-3450
Titre abrégé: J Am Soc Nephrol
Pays: United States
ID NLM: 9013836

Informations de publication

Date de publication:
07 2020
Historique:
received: 28 08 2019
accepted: 22 03 2020
pubmed: 3 6 2020
medline: 25 2 2021
entrez: 3 6 2020
Statut: ppublish

Résumé

Short-chain fatty acids derived from gut microbial fermentation of dietary fiber have been shown to suppress autoimmunity through mechanisms that include enhanced regulation by T regulatory cells (Tregs). Using a murine kidney transplantation model, we examined the effects on alloimmunity of a high-fiber diet or supplementation with the short-chain fatty acid acetate. Kidney transplants were performed from BALB/c(H2 Wild-type mice fed normal chow exhibited dysbiosis after receiving a kidney allograft but not an isograft, despite the avoidance of antibiotics and immunosuppression for the latter. A high-fiber diet prevented dysbiosis in allograft recipients, who demonstrated prolonged survival and reduced evidence of rejection compared with mice fed normal chow. Allograft mice receiving supplemental sodium acetate exhibited similar protection from rejection, and subsequently demonstrated donor-specific tolerance. Depletion of CD25 Manipulation of the microbiome by a high-fiber diet or supplementation with sodium acetate modified alloimmunity in a kidney transplant model, generating tolerance dependent on Tregs and GPR43. Diet-based therapy to induce changes in the gut microbiome can alter systemic alloimmunity in mice, in part through the production of short-chain fatty acids leading to Treg cell development, and merits study as a potential clinical strategy to facilitate transplant acceptance.

Sections du résumé

BACKGROUND
Short-chain fatty acids derived from gut microbial fermentation of dietary fiber have been shown to suppress autoimmunity through mechanisms that include enhanced regulation by T regulatory cells (Tregs).
METHODS
Using a murine kidney transplantation model, we examined the effects on alloimmunity of a high-fiber diet or supplementation with the short-chain fatty acid acetate. Kidney transplants were performed from BALB/c(H2
RESULTS
Wild-type mice fed normal chow exhibited dysbiosis after receiving a kidney allograft but not an isograft, despite the avoidance of antibiotics and immunosuppression for the latter. A high-fiber diet prevented dysbiosis in allograft recipients, who demonstrated prolonged survival and reduced evidence of rejection compared with mice fed normal chow. Allograft mice receiving supplemental sodium acetate exhibited similar protection from rejection, and subsequently demonstrated donor-specific tolerance. Depletion of CD25
CONCLUSIONS
Manipulation of the microbiome by a high-fiber diet or supplementation with sodium acetate modified alloimmunity in a kidney transplant model, generating tolerance dependent on Tregs and GPR43. Diet-based therapy to induce changes in the gut microbiome can alter systemic alloimmunity in mice, in part through the production of short-chain fatty acids leading to Treg cell development, and merits study as a potential clinical strategy to facilitate transplant acceptance.

Identifiants

pubmed: 32482686
pii: ASN.2019080852
doi: 10.1681/ASN.2019080852
pmc: PMC7350991
doi:

Substances chimiques

Dietary Fiber 0
Fatty Acids, Volatile 0
Ffar2 protein, mouse 0
Receptors, G-Protein-Coupled 0
Butyric Acid 107-92-6
Sodium Acetate 4550K0SC9B

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1445-1461

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 by the American Society of Nephrology.

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Auteurs

Huiling Wu (H)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia huiling.wu@sydney.edu.au.
Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia.

Julian Singer (J)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.
Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.

Tony K Kwan (TK)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.
Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.

Yik Wen Loh (YW)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.
Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.

Chuanmin Wang (C)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.
Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.

Jian Tan (J)

Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
Nutritional Immunometabolism Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.

Yan J Li (YJ)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia huiling.wu@sydney.edu.au.

Sum Wing Christina Lai (SWC)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.

Laurence Macia (L)

Nutritional Immunometabolism Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.
School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.

Stephen I Alexander (SI)

Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
Centre for Kidney Research, The Children's Hospital at Westmead, Westmead, New South Wales, Australia.

Steven J Chadban (SJ)

Kidney Node Laboratory, The Charles Perkins Centre, Camperdown, New South Wales, Australia.
Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia.

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Classifications MeSH