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The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial
IgA secretion at mucosal sites is important for host defence against pathogens as well as maintaining the symbiosis with microorganisms present in the small intestine that affect IgA production. In the present study, we tested the ability of 5 strains of lactic acid bacteria stimulating IgA producti...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5864838/ https://www.ncbi.nlm.nih.gov/pubmed/29567956 http://dx.doi.org/10.1038/s41598-018-23404-4 |
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author | Kawashima, Tadaomi Ikari, Naho Kouchi, Tomoko Kowatari, Yasuyuki Kubota, Yoshiro Shimojo, Naoki Tsuji, Noriko M. |
author_facet | Kawashima, Tadaomi Ikari, Naho Kouchi, Tomoko Kowatari, Yasuyuki Kubota, Yoshiro Shimojo, Naoki Tsuji, Noriko M. |
author_sort | Kawashima, Tadaomi |
collection | PubMed |
description | IgA secretion at mucosal sites is important for host defence against pathogens as well as maintaining the symbiosis with microorganisms present in the small intestine that affect IgA production. In the present study, we tested the ability of 5 strains of lactic acid bacteria stimulating IgA production, being Pediococcus acidilactici K15 selected as the most effective on inducing this protective immunoglobulin. We found that this response was mainly induced via IL-10, as efficiently as IL-6, secreted by K15-stimulated dendritic cells. Furthermore, bacterial RNA was largely responsible for the induction of these cytokines; double-stranded RNA was a major causative molecule for IL-6 production whereas single-stranded RNA was critical factor for IL-10 production. In a randomized, double-blind, placebo-controlled clinical trial, ingestion of K15 significantly increased the secretory IgA (sIgA) concentration in saliva compared with the basal level observed before this intervention. These results indicate that functional lactic acid bacteria induce IL-6 and IL-10 production by dendritic cells, which contribute to upregulating the sIgA concentration at mucosal sites in humans. |
format | Online Article Text |
id | pubmed-5864838 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58648382018-03-27 The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial Kawashima, Tadaomi Ikari, Naho Kouchi, Tomoko Kowatari, Yasuyuki Kubota, Yoshiro Shimojo, Naoki Tsuji, Noriko M. Sci Rep Article IgA secretion at mucosal sites is important for host defence against pathogens as well as maintaining the symbiosis with microorganisms present in the small intestine that affect IgA production. In the present study, we tested the ability of 5 strains of lactic acid bacteria stimulating IgA production, being Pediococcus acidilactici K15 selected as the most effective on inducing this protective immunoglobulin. We found that this response was mainly induced via IL-10, as efficiently as IL-6, secreted by K15-stimulated dendritic cells. Furthermore, bacterial RNA was largely responsible for the induction of these cytokines; double-stranded RNA was a major causative molecule for IL-6 production whereas single-stranded RNA was critical factor for IL-10 production. In a randomized, double-blind, placebo-controlled clinical trial, ingestion of K15 significantly increased the secretory IgA (sIgA) concentration in saliva compared with the basal level observed before this intervention. These results indicate that functional lactic acid bacteria induce IL-6 and IL-10 production by dendritic cells, which contribute to upregulating the sIgA concentration at mucosal sites in humans. Nature Publishing Group UK 2018-03-22 /pmc/articles/PMC5864838/ /pubmed/29567956 http://dx.doi.org/10.1038/s41598-018-23404-4 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Kawashima, Tadaomi Ikari, Naho Kouchi, Tomoko Kowatari, Yasuyuki Kubota, Yoshiro Shimojo, Naoki Tsuji, Noriko M. The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial |
title | The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial |
title_full | The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial |
title_fullStr | The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial |
title_full_unstemmed | The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial |
title_short | The molecular mechanism for activating IgA production by Pediococcus acidilactici K15 and the clinical impact in a randomized trial |
title_sort | molecular mechanism for activating iga production by pediococcus acidilactici k15 and the clinical impact in a randomized trial |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5864838/ https://www.ncbi.nlm.nih.gov/pubmed/29567956 http://dx.doi.org/10.1038/s41598-018-23404-4 |
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