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To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease
Celiac disease (CD) is an immune-mediated disorder triggered by the ingestion of gluten and characterized by reversible small-bowel mucosal atrophy in genetically predisposed subjects. Although the prevalence of CD has increased, many aspects of this pathology are still unrecognized. Candida albican...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906151/ https://www.ncbi.nlm.nih.gov/pubmed/31867008 http://dx.doi.org/10.3389/fimmu.2019.02844 |
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author | Renga, Giorgia Bellet, Marina M. Stincardini, Claudia Pariano, Marilena Oikonomou, Vasilis Villella, Valeria R. Brancorsini, Stefano Clerici, Carlo Romani, Luigina Costantini, Claudio |
author_facet | Renga, Giorgia Bellet, Marina M. Stincardini, Claudia Pariano, Marilena Oikonomou, Vasilis Villella, Valeria R. Brancorsini, Stefano Clerici, Carlo Romani, Luigina Costantini, Claudio |
author_sort | Renga, Giorgia |
collection | PubMed |
description | Celiac disease (CD) is an immune-mediated disorder triggered by the ingestion of gluten and characterized by reversible small-bowel mucosal atrophy in genetically predisposed subjects. Although the prevalence of CD has increased, many aspects of this pathology are still unrecognized. Candida albicans, a commensal of the human gastrointestinal tract, has been linked to CD for a long time based, among others, upon the observation of similarity between the fungal wall component, hyphal wall protein 1, and CD-related gliadin T-cell epitopes. We have recently demonstrated that Candida may switch from commensal to pathogen contingent upon several players, including mast cells, key sentinels of the immune system at the interface between the environment and the host, and the pleiotropic cytokine IL-9. However, other factors are likely to play a role by altering the balance between inflammation and tolerance. In this regard, tryptophan and its metabolites are increasingly being recognized in promoting mucosal homeostasis by balancing the immune response to external cues. Based on these premises, we will discuss how the output of Candida colonization in the gut is highly contextual, being determined at the intersection of many immunological (IL-9/mast cells) and metabolic (tryptophan) pathways that ultimately dictate the Candida commensalism vs. pathogenicity in CD, thus paving the way for novel therapeutic opportunities in CD. |
format | Online Article Text |
id | pubmed-6906151 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-69061512019-12-20 To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease Renga, Giorgia Bellet, Marina M. Stincardini, Claudia Pariano, Marilena Oikonomou, Vasilis Villella, Valeria R. Brancorsini, Stefano Clerici, Carlo Romani, Luigina Costantini, Claudio Front Immunol Immunology Celiac disease (CD) is an immune-mediated disorder triggered by the ingestion of gluten and characterized by reversible small-bowel mucosal atrophy in genetically predisposed subjects. Although the prevalence of CD has increased, many aspects of this pathology are still unrecognized. Candida albicans, a commensal of the human gastrointestinal tract, has been linked to CD for a long time based, among others, upon the observation of similarity between the fungal wall component, hyphal wall protein 1, and CD-related gliadin T-cell epitopes. We have recently demonstrated that Candida may switch from commensal to pathogen contingent upon several players, including mast cells, key sentinels of the immune system at the interface between the environment and the host, and the pleiotropic cytokine IL-9. However, other factors are likely to play a role by altering the balance between inflammation and tolerance. In this regard, tryptophan and its metabolites are increasingly being recognized in promoting mucosal homeostasis by balancing the immune response to external cues. Based on these premises, we will discuss how the output of Candida colonization in the gut is highly contextual, being determined at the intersection of many immunological (IL-9/mast cells) and metabolic (tryptophan) pathways that ultimately dictate the Candida commensalism vs. pathogenicity in CD, thus paving the way for novel therapeutic opportunities in CD. Frontiers Media S.A. 2019-12-05 /pmc/articles/PMC6906151/ /pubmed/31867008 http://dx.doi.org/10.3389/fimmu.2019.02844 Text en Copyright © 2019 Renga, Bellet, Stincardini, Pariano, Oikonomou, Villella, Brancorsini, Clerici, Romani and Costantini. 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 Renga, Giorgia Bellet, Marina M. Stincardini, Claudia Pariano, Marilena Oikonomou, Vasilis Villella, Valeria R. Brancorsini, Stefano Clerici, Carlo Romani, Luigina Costantini, Claudio To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease |
title | To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease |
title_full | To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease |
title_fullStr | To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease |
title_full_unstemmed | To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease |
title_short | To Be or Not to Be a Pathogen: Candida albicans and Celiac Disease |
title_sort | to be or not to be a pathogen: candida albicans and celiac disease |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906151/ https://www.ncbi.nlm.nih.gov/pubmed/31867008 http://dx.doi.org/10.3389/fimmu.2019.02844 |
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