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Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies

Food allergy is an atopic disease that is caused by the immune system targeting harmless food antigens that can result in life-threatening anaphylaxis. As humans and microbes have co-evolved, inevitably commensal microbes have a tremendous impact on our health. As such, the gut with its enormous mic...

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Autores principales: Kreft, Luisa, Hoffmann, Christian, Ohnmacht, Caspar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7456891/
https://www.ncbi.nlm.nih.gov/pubmed/32922400
http://dx.doi.org/10.3389/fimmu.2020.01853
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author Kreft, Luisa
Hoffmann, Christian
Ohnmacht, Caspar
author_facet Kreft, Luisa
Hoffmann, Christian
Ohnmacht, Caspar
author_sort Kreft, Luisa
collection PubMed
description Food allergy is an atopic disease that is caused by the immune system targeting harmless food antigens that can result in life-threatening anaphylaxis. As humans and microbes have co-evolved, inevitably commensal microbes have a tremendous impact on our health. As such, the gut with its enormous microbial richness reflects a highly tolerogenic environment at steady state, in which immune cells are educated to react in a well-calibrated manner to food and microbial antigens. Recent evidence indicates that the susceptibility to food allergy is critically linked to microbial dysbiosis and can be transmitted by microbial transfer from humans to mice. Experimental work and epidemiological studies further point toward a critical time window in early childhood during which the immune system is imprinted by microbial colonization. Particularly, Foxp3-expressing regulatory T cells turn out to be key players, acting as rheostats for controlling the magnitude of food allergic reactions. An increasing number of bacterial metabolites has recently been shown to regulate directly or indirectly the differentiation of peripherally induced Tregs, most of which co-express the RAR-related orphan receptor gamma t (RORγt). Genetic ablation provided additional direct evidence for the importance of RORγt+ Tregs in food allergy. Future strategies for the stratification of food allergic patients with the aim to manipulate the intestinal microbiota by means of fecal transplantation efforts, pre- or probiotic regimens or for boosting oral immunotherapy may improve diagnosis and therapy. In this review some of the key underlying mechanisms are summarized and future directions for potential microbial therapy are explored.
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spelling pubmed-74568912020-09-11 Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies Kreft, Luisa Hoffmann, Christian Ohnmacht, Caspar Front Immunol Immunology Food allergy is an atopic disease that is caused by the immune system targeting harmless food antigens that can result in life-threatening anaphylaxis. As humans and microbes have co-evolved, inevitably commensal microbes have a tremendous impact on our health. As such, the gut with its enormous microbial richness reflects a highly tolerogenic environment at steady state, in which immune cells are educated to react in a well-calibrated manner to food and microbial antigens. Recent evidence indicates that the susceptibility to food allergy is critically linked to microbial dysbiosis and can be transmitted by microbial transfer from humans to mice. Experimental work and epidemiological studies further point toward a critical time window in early childhood during which the immune system is imprinted by microbial colonization. Particularly, Foxp3-expressing regulatory T cells turn out to be key players, acting as rheostats for controlling the magnitude of food allergic reactions. An increasing number of bacterial metabolites has recently been shown to regulate directly or indirectly the differentiation of peripherally induced Tregs, most of which co-express the RAR-related orphan receptor gamma t (RORγt). Genetic ablation provided additional direct evidence for the importance of RORγt+ Tregs in food allergy. Future strategies for the stratification of food allergic patients with the aim to manipulate the intestinal microbiota by means of fecal transplantation efforts, pre- or probiotic regimens or for boosting oral immunotherapy may improve diagnosis and therapy. In this review some of the key underlying mechanisms are summarized and future directions for potential microbial therapy are explored. Frontiers Media S.A. 2020-08-14 /pmc/articles/PMC7456891/ /pubmed/32922400 http://dx.doi.org/10.3389/fimmu.2020.01853 Text en Copyright © 2020 Kreft, Hoffmann and Ohnmacht. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Kreft, Luisa
Hoffmann, Christian
Ohnmacht, Caspar
Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies
title Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies
title_full Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies
title_fullStr Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies
title_full_unstemmed Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies
title_short Therapeutic Potential of the Intestinal Microbiota for Immunomodulation of Food Allergies
title_sort therapeutic potential of the intestinal microbiota for immunomodulation of food allergies
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7456891/
https://www.ncbi.nlm.nih.gov/pubmed/32922400
http://dx.doi.org/10.3389/fimmu.2020.01853
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