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W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota
W27 monoclonal immunoglobulin A (IgA) suppresses pathogenic Escherichia coli cell growth; however, its effect on the human intestine remains unclear. We aimed to determine how W27 IgA affects the human colonic microbiota using the in vitro microbiota model. This model was established using fecal sam...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8285510/ https://www.ncbi.nlm.nih.gov/pubmed/34272464 http://dx.doi.org/10.1038/s41598-021-94210-8 |
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author | Sasaki, Kengo Mori, Tomoyuki Hoshi, Namiko Sasaki, Daisuke Inoue, Jun Shinkura, Reiko Kondo, Akihiko |
author_facet | Sasaki, Kengo Mori, Tomoyuki Hoshi, Namiko Sasaki, Daisuke Inoue, Jun Shinkura, Reiko Kondo, Akihiko |
author_sort | Sasaki, Kengo |
collection | PubMed |
description | W27 monoclonal immunoglobulin A (IgA) suppresses pathogenic Escherichia coli cell growth; however, its effect on the human intestine remains unclear. We aimed to determine how W27 IgA affects the human colonic microbiota using the in vitro microbiota model. This model was established using fecal samples collected from 12 healthy volunteers; after anaerobic cultivation, each model was found to retain the genera found in the original human fecal samples. After pre-incubating W27 IgA with the respective fecal sample under aerobic conditions, the mixture of W27 IgA (final concentration, 0.5 μg/mL) and each fecal sample was added to the in vitro microbiota model and cultured under anaerobic conditions. Next-generation sequencing of the bacterial 16S rRNA gene revealed that W27 IgA significantly decreased the relative abundance of bacteria related to the genus Escherichia in the model. Additionally, at a final concentration of 5 μg/mL, W27 IgA delayed growth in the pure culture of Escherichia coli isolated from human fecal samples. Our study thus revealed the suppressive effect of W27 IgA on the genus Escherichia at relatively low-concentrations and the usefulness of an in vitro microbiota model to evaluate the effect of IgA as a gut microbiota regulator. |
format | Online Article Text |
id | pubmed-8285510 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-82855102021-07-19 W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota Sasaki, Kengo Mori, Tomoyuki Hoshi, Namiko Sasaki, Daisuke Inoue, Jun Shinkura, Reiko Kondo, Akihiko Sci Rep Article W27 monoclonal immunoglobulin A (IgA) suppresses pathogenic Escherichia coli cell growth; however, its effect on the human intestine remains unclear. We aimed to determine how W27 IgA affects the human colonic microbiota using the in vitro microbiota model. This model was established using fecal samples collected from 12 healthy volunteers; after anaerobic cultivation, each model was found to retain the genera found in the original human fecal samples. After pre-incubating W27 IgA with the respective fecal sample under aerobic conditions, the mixture of W27 IgA (final concentration, 0.5 μg/mL) and each fecal sample was added to the in vitro microbiota model and cultured under anaerobic conditions. Next-generation sequencing of the bacterial 16S rRNA gene revealed that W27 IgA significantly decreased the relative abundance of bacteria related to the genus Escherichia in the model. Additionally, at a final concentration of 5 μg/mL, W27 IgA delayed growth in the pure culture of Escherichia coli isolated from human fecal samples. Our study thus revealed the suppressive effect of W27 IgA on the genus Escherichia at relatively low-concentrations and the usefulness of an in vitro microbiota model to evaluate the effect of IgA as a gut microbiota regulator. Nature Publishing Group UK 2021-07-16 /pmc/articles/PMC8285510/ /pubmed/34272464 http://dx.doi.org/10.1038/s41598-021-94210-8 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Sasaki, Kengo Mori, Tomoyuki Hoshi, Namiko Sasaki, Daisuke Inoue, Jun Shinkura, Reiko Kondo, Akihiko W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota |
title | W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota |
title_full | W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota |
title_fullStr | W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota |
title_full_unstemmed | W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota |
title_short | W27 IgA suppresses growth of Escherichia in an in vitro model of the human intestinal microbiota |
title_sort | w27 iga suppresses growth of escherichia in an in vitro model of the human intestinal microbiota |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8285510/ https://www.ncbi.nlm.nih.gov/pubmed/34272464 http://dx.doi.org/10.1038/s41598-021-94210-8 |
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