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Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action

Epithelial damage and loss of barrier integrity occur following intestinal infections in humans and animals. Gut health was evaluated by electron microscopy in an avian model that exposed birds to subclinical necrotic enteritis (NE) and fed them a diet supplemented with the probiotic Bacillus amylol...

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Autores principales: Shini, Shaniko, Aland, R. Claire, Bryden, Wayne L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7794591/
https://www.ncbi.nlm.nih.gov/pubmed/33420315
http://dx.doi.org/10.1038/s41598-020-80714-2
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author Shini, Shaniko
Aland, R. Claire
Bryden, Wayne L.
author_facet Shini, Shaniko
Aland, R. Claire
Bryden, Wayne L.
author_sort Shini, Shaniko
collection PubMed
description Epithelial damage and loss of barrier integrity occur following intestinal infections in humans and animals. Gut health was evaluated by electron microscopy in an avian model that exposed birds to subclinical necrotic enteritis (NE) and fed them a diet supplemented with the probiotic Bacillus amyloliquefaciens strain H57 (H57). Scanning electron microscopy of ileal mucosa revealed significant villus damage, including focal erosions of epithelial cells and villous atrophy, while transmission electron microscopy demonstrated severe enterocyte damage and loss of cellular integrity in NE-exposed birds. In particular, mitochondria were morphologically altered, appearing irregular in shape or swollen, and containing electron-lucent regions of matrix and damaged cristae. Apical junctional complexes between adjacent enterocytes were significantly shorter, and the adherens junction was saccular, suggesting loss of epithelial integrity in NE birds. Segmented filamentous bacteria attached to villi, which play an important role in intestinal immunity, were more numerous in birds exposed to NE. The results suggest that mitochondrial damage may be an important initiator of NE pathogenesis, while H57 maintains epithelium and improves the integrity of intestinal mucosa. Potential actions of H57 are discussed that further define the mechanisms responsible for probiotic bacteria’s role in maintaining gut health.
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spelling pubmed-77945912021-01-12 Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action Shini, Shaniko Aland, R. Claire Bryden, Wayne L. Sci Rep Article Epithelial damage and loss of barrier integrity occur following intestinal infections in humans and animals. Gut health was evaluated by electron microscopy in an avian model that exposed birds to subclinical necrotic enteritis (NE) and fed them a diet supplemented with the probiotic Bacillus amyloliquefaciens strain H57 (H57). Scanning electron microscopy of ileal mucosa revealed significant villus damage, including focal erosions of epithelial cells and villous atrophy, while transmission electron microscopy demonstrated severe enterocyte damage and loss of cellular integrity in NE-exposed birds. In particular, mitochondria were morphologically altered, appearing irregular in shape or swollen, and containing electron-lucent regions of matrix and damaged cristae. Apical junctional complexes between adjacent enterocytes were significantly shorter, and the adherens junction was saccular, suggesting loss of epithelial integrity in NE birds. Segmented filamentous bacteria attached to villi, which play an important role in intestinal immunity, were more numerous in birds exposed to NE. The results suggest that mitochondrial damage may be an important initiator of NE pathogenesis, while H57 maintains epithelium and improves the integrity of intestinal mucosa. Potential actions of H57 are discussed that further define the mechanisms responsible for probiotic bacteria’s role in maintaining gut health. Nature Publishing Group UK 2021-01-08 /pmc/articles/PMC7794591/ /pubmed/33420315 http://dx.doi.org/10.1038/s41598-020-80714-2 Text en © The Author(s) 2021 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/.
spellingShingle Article
Shini, Shaniko
Aland, R. Claire
Bryden, Wayne L.
Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
title Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
title_full Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
title_fullStr Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
title_full_unstemmed Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
title_short Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
title_sort avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7794591/
https://www.ncbi.nlm.nih.gov/pubmed/33420315
http://dx.doi.org/10.1038/s41598-020-80714-2
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