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Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood
Development of the intestinal microbiota during early life serves a key regulatory stage in establishing the host-microbial relationship. This symbiotic relationship contributes to developing host immunity and maintaining health throughout the life span. This study was to develop an approach to colo...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5073052/ https://www.ncbi.nlm.nih.gov/pubmed/27095077 http://dx.doi.org/10.1038/mi.2016.43 |
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author | Yan, Fang Liu, Liping Cao, Hailong Moore, Daniel J. Washington, M. Kay Wang, Bangmao Peek, Richard M. Acra, Sari A. Polk, D. Brent |
author_facet | Yan, Fang Liu, Liping Cao, Hailong Moore, Daniel J. Washington, M. Kay Wang, Bangmao Peek, Richard M. Acra, Sari A. Polk, D. Brent |
author_sort | Yan, Fang |
collection | PubMed |
description | Development of the intestinal microbiota during early life serves a key regulatory stage in establishing the host-microbial relationship. This symbiotic relationship contributes to developing host immunity and maintaining health throughout the life span. This study was to develop an approach to colonize conventionally raised mice with a model probiotic bacterium, Lactobacillus rhamnosus GG (LGG), and determine the effects of LGG colonization on intestinal development and prevention of colitis in adulthood. LGG colonization in conventionally raised was established by administering LGG to pregnant mice starting at gestational day 18 and pups at postnatal day 1 to day 5. LGG colonization promoted bodyweight gain and increased diversity and richness of the colonic mucosa-associated microbiota prior to weaning. Intestinal epithelial cell proliferation, differentiation, tight junction formation and mucosal IgA production were all significantly enhanced in LGG colonized mice. Adult mice colonized with LGG showed increased IgA production and decreased susceptibility to intestinal injury and inflammation induced in the dextran sodium sulphate model of colitis. Thus, neonatal colonization of mice with LGG enhances intestinal functional maturation and IgA production and confers life long health consequences on protection from intestinal injury and inflammation. This strategy might be applied for benefiting health in the host. |
format | Online Article Text |
id | pubmed-5073052 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
record_format | MEDLINE/PubMed |
spelling | pubmed-50730522016-10-21 Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood Yan, Fang Liu, Liping Cao, Hailong Moore, Daniel J. Washington, M. Kay Wang, Bangmao Peek, Richard M. Acra, Sari A. Polk, D. Brent Mucosal Immunol Article Development of the intestinal microbiota during early life serves a key regulatory stage in establishing the host-microbial relationship. This symbiotic relationship contributes to developing host immunity and maintaining health throughout the life span. This study was to develop an approach to colonize conventionally raised mice with a model probiotic bacterium, Lactobacillus rhamnosus GG (LGG), and determine the effects of LGG colonization on intestinal development and prevention of colitis in adulthood. LGG colonization in conventionally raised was established by administering LGG to pregnant mice starting at gestational day 18 and pups at postnatal day 1 to day 5. LGG colonization promoted bodyweight gain and increased diversity and richness of the colonic mucosa-associated microbiota prior to weaning. Intestinal epithelial cell proliferation, differentiation, tight junction formation and mucosal IgA production were all significantly enhanced in LGG colonized mice. Adult mice colonized with LGG showed increased IgA production and decreased susceptibility to intestinal injury and inflammation induced in the dextran sodium sulphate model of colitis. Thus, neonatal colonization of mice with LGG enhances intestinal functional maturation and IgA production and confers life long health consequences on protection from intestinal injury and inflammation. This strategy might be applied for benefiting health in the host. 2016-04-20 2017-01 /pmc/articles/PMC5073052/ /pubmed/27095077 http://dx.doi.org/10.1038/mi.2016.43 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Yan, Fang Liu, Liping Cao, Hailong Moore, Daniel J. Washington, M. Kay Wang, Bangmao Peek, Richard M. Acra, Sari A. Polk, D. Brent Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood |
title | Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood |
title_full | Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood |
title_fullStr | Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood |
title_full_unstemmed | Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood |
title_short | Neonatal Colonization of Mice with LGG Promotes Intestinal Development and Decreases Susceptibility to Colitis in Adulthood |
title_sort | neonatal colonization of mice with lgg promotes intestinal development and decreases susceptibility to colitis in adulthood |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5073052/ https://www.ncbi.nlm.nih.gov/pubmed/27095077 http://dx.doi.org/10.1038/mi.2016.43 |
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