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Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity
Exposure to gluten, a protein present in wheat rye and barley, is the major inducer for human Celiac Disease (CD), a chronic autoimmune enteropathy. CD occurs in about 1% worldwide population, in genetically predisposed individuals bearing human leukocyte antigen (HLA) DQ2/DQ8. Gut epithelial cell s...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8067866/ https://www.ncbi.nlm.nih.gov/pubmed/33917155 http://dx.doi.org/10.3390/nu13041221 |
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author | Ferrari, Eleonora Monzani, Romina Saverio, Valentina Gagliardi, Mara Pańczyszyn, Elżbieta Raia, Valeria Villella, Valeria Rachela Bona, Gianni Pane, Marco Amoruso, Angela Corazzari, Marco |
author_facet | Ferrari, Eleonora Monzani, Romina Saverio, Valentina Gagliardi, Mara Pańczyszyn, Elżbieta Raia, Valeria Villella, Valeria Rachela Bona, Gianni Pane, Marco Amoruso, Angela Corazzari, Marco |
author_sort | Ferrari, Eleonora |
collection | PubMed |
description | Exposure to gluten, a protein present in wheat rye and barley, is the major inducer for human Celiac Disease (CD), a chronic autoimmune enteropathy. CD occurs in about 1% worldwide population, in genetically predisposed individuals bearing human leukocyte antigen (HLA) DQ2/DQ8. Gut epithelial cell stress and the innate immune activation are responsible for the breaking oral tolerance to gliadin, a gluten component. To date, the only treatment available for CD is a long-term gluten-free diet. Several studies have shown that an altered composition of the intestinal microbiota (dysbiosis) could play a key role in the pathogenesis of CD through the modulation of intestinal permeability and the regulation of the immune system. Here, we show that gliadin induces a chronic endoplasmic reticulum (ER) stress condition in the small intestine of a gluten-sensitive mouse model and that the coadministration of probiotics efficiently attenuates both the unfolded protein response (UPR) and gut inflammation. Moreover, the composition of probiotics formulations might differ in their activity at molecular level, especially toward the three axes of the UPR. Therefore, probiotics administration might potentially represent a new valuable strategy to treat gluten-sensitive patients, such as those affected by CD. |
format | Online Article Text |
id | pubmed-8067866 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-80678662021-04-25 Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity Ferrari, Eleonora Monzani, Romina Saverio, Valentina Gagliardi, Mara Pańczyszyn, Elżbieta Raia, Valeria Villella, Valeria Rachela Bona, Gianni Pane, Marco Amoruso, Angela Corazzari, Marco Nutrients Article Exposure to gluten, a protein present in wheat rye and barley, is the major inducer for human Celiac Disease (CD), a chronic autoimmune enteropathy. CD occurs in about 1% worldwide population, in genetically predisposed individuals bearing human leukocyte antigen (HLA) DQ2/DQ8. Gut epithelial cell stress and the innate immune activation are responsible for the breaking oral tolerance to gliadin, a gluten component. To date, the only treatment available for CD is a long-term gluten-free diet. Several studies have shown that an altered composition of the intestinal microbiota (dysbiosis) could play a key role in the pathogenesis of CD through the modulation of intestinal permeability and the regulation of the immune system. Here, we show that gliadin induces a chronic endoplasmic reticulum (ER) stress condition in the small intestine of a gluten-sensitive mouse model and that the coadministration of probiotics efficiently attenuates both the unfolded protein response (UPR) and gut inflammation. Moreover, the composition of probiotics formulations might differ in their activity at molecular level, especially toward the three axes of the UPR. Therefore, probiotics administration might potentially represent a new valuable strategy to treat gluten-sensitive patients, such as those affected by CD. MDPI 2021-04-07 /pmc/articles/PMC8067866/ /pubmed/33917155 http://dx.doi.org/10.3390/nu13041221 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Ferrari, Eleonora Monzani, Romina Saverio, Valentina Gagliardi, Mara Pańczyszyn, Elżbieta Raia, Valeria Villella, Valeria Rachela Bona, Gianni Pane, Marco Amoruso, Angela Corazzari, Marco Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity |
title | Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity |
title_full | Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity |
title_fullStr | Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity |
title_full_unstemmed | Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity |
title_short | Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity |
title_sort | probiotics supplements reduce er stress and gut inflammation associated with gliadin intake in a mouse model of gluten sensitivity |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8067866/ https://www.ncbi.nlm.nih.gov/pubmed/33917155 http://dx.doi.org/10.3390/nu13041221 |
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