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Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes in the intestinal environment in mice
We investigated the effect of resistant maltodextrin (RMD), a non-viscous soluble dietary fiber, on intestinal immune response and its mechanism in mice. Intestinal and fecal immunoglobulin A (IgA) were determined as indicators of intestinal immune response, and changes in the intestinal environment...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMFH Press
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4735028/ https://www.ncbi.nlm.nih.gov/pubmed/26858925 http://dx.doi.org/10.12938/bmfh.2015-009 |
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author | MIYAZATO, Shoko KISHIMOTO, Yuka TAKAHASHI, Kyoko KAMINOGAWA, Shuichi HOSONO, Akira |
author_facet | MIYAZATO, Shoko KISHIMOTO, Yuka TAKAHASHI, Kyoko KAMINOGAWA, Shuichi HOSONO, Akira |
author_sort | MIYAZATO, Shoko |
collection | PubMed |
description | We investigated the effect of resistant maltodextrin (RMD), a non-viscous soluble dietary fiber, on intestinal immune response and its mechanism in mice. Intestinal and fecal immunoglobulin A (IgA) were determined as indicators of intestinal immune response, and changes in the intestinal environment were focused to study the mechanism. BALB/c mice were fed one of three experimental diets, a control diet or a diet containing either 5% or 7.5% RMD, for two weeks. Continuous intake of RMD dose-dependently increased total IgA levels in the intestinal tract. Total IgA production from the cecal mucosa was significantly increased by RMD intake, while there were no significant differences in mucosal IgA production between the control group and experimental groups in the small intestine and colon. Continuous intake of RMD changed the composition of the cecal contents; that is, the composition of the cecal microbiota was changed, and short-chain fatty acids (SCFAs) were increased. There was an increased trend in Bacteroidales in the cecal microbiota, and butyrate, an SCFA, was significantly increased. Our study demonstrated that continuous intake of RMD enhanced the intestinal immune response by increasing the production of IgA in the intestinal tract. It suggested that the increase in total SCFAs and changes in the intestinal microbiota resulting from the fermentation of RMD orally ingested were associated with the induction of IgA production in intestinal immune cells, with the IgA production of the cecal mucosa in particular being significantly increased. |
format | Online Article Text |
id | pubmed-4735028 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BMFH Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-47350282016-02-08 Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes in the intestinal environment in mice MIYAZATO, Shoko KISHIMOTO, Yuka TAKAHASHI, Kyoko KAMINOGAWA, Shuichi HOSONO, Akira Biosci Microbiota Food Health Full Paper We investigated the effect of resistant maltodextrin (RMD), a non-viscous soluble dietary fiber, on intestinal immune response and its mechanism in mice. Intestinal and fecal immunoglobulin A (IgA) were determined as indicators of intestinal immune response, and changes in the intestinal environment were focused to study the mechanism. BALB/c mice were fed one of three experimental diets, a control diet or a diet containing either 5% or 7.5% RMD, for two weeks. Continuous intake of RMD dose-dependently increased total IgA levels in the intestinal tract. Total IgA production from the cecal mucosa was significantly increased by RMD intake, while there were no significant differences in mucosal IgA production between the control group and experimental groups in the small intestine and colon. Continuous intake of RMD changed the composition of the cecal contents; that is, the composition of the cecal microbiota was changed, and short-chain fatty acids (SCFAs) were increased. There was an increased trend in Bacteroidales in the cecal microbiota, and butyrate, an SCFA, was significantly increased. Our study demonstrated that continuous intake of RMD enhanced the intestinal immune response by increasing the production of IgA in the intestinal tract. It suggested that the increase in total SCFAs and changes in the intestinal microbiota resulting from the fermentation of RMD orally ingested were associated with the induction of IgA production in intestinal immune cells, with the IgA production of the cecal mucosa in particular being significantly increased. BMFH Press 2015-08-25 2016 /pmc/articles/PMC4735028/ /pubmed/26858925 http://dx.doi.org/10.12938/bmfh.2015-009 Text en BMFH Press http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. |
spellingShingle | Full Paper MIYAZATO, Shoko KISHIMOTO, Yuka TAKAHASHI, Kyoko KAMINOGAWA, Shuichi HOSONO, Akira Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes in the intestinal environment in mice |
title | Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes
in the intestinal environment in mice |
title_full | Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes
in the intestinal environment in mice |
title_fullStr | Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes
in the intestinal environment in mice |
title_full_unstemmed | Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes
in the intestinal environment in mice |
title_short | Continuous intake of resistant maltodextrin enhanced intestinal immune response through changes
in the intestinal environment in mice |
title_sort | continuous intake of resistant maltodextrin enhanced intestinal immune response through changes
in the intestinal environment in mice |
topic | Full Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4735028/ https://www.ncbi.nlm.nih.gov/pubmed/26858925 http://dx.doi.org/10.12938/bmfh.2015-009 |
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