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Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier
The small intestinal mucosa constitutes a physical barrier separating the gut lumen from sterile internal tissues. Junctional complexes between cells regulate transport across the barrier, preventing water loss and the entry of noxious molecules or pathogens. Inflammatory diseases in cattle disrupt...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9418144/ https://www.ncbi.nlm.nih.gov/pubmed/36028741 http://dx.doi.org/10.1038/s41598-022-18771-y |
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author | Crawford, Charles K. Lopez Cervantes, Veronica Quilici, Mary L. Armién, Aníbal G. Questa, María Matloob, Muhammad S. Huynh, Leon D. Beltran, Aeelin Karchemskiy, Sophie J. Crakes, Katti R. Kol, Amir |
author_facet | Crawford, Charles K. Lopez Cervantes, Veronica Quilici, Mary L. Armién, Aníbal G. Questa, María Matloob, Muhammad S. Huynh, Leon D. Beltran, Aeelin Karchemskiy, Sophie J. Crakes, Katti R. Kol, Amir |
author_sort | Crawford, Charles K. |
collection | PubMed |
description | The small intestinal mucosa constitutes a physical barrier separating the gut lumen from sterile internal tissues. Junctional complexes between cells regulate transport across the barrier, preventing water loss and the entry of noxious molecules or pathogens. Inflammatory diseases in cattle disrupt this barrier; nonetheless, mechanisms of barrier disruption in cattle are poorly understood. We investigated the direct effects of three inflammatory cytokines, TNFα, IFNγ, and IL-18, on the bovine intestinal barrier utilizing intestinal organoids. Flux of fluorescein isothiocyanate (FITC)-labeled dextran was used to investigate barrier permeability. Immunocytochemistry and transmission electron microscopy were used to investigate junctional morphology, specifically tortuosity and length/width, respectively. Immunocytochemistry and flow cytometry was used to investigate cellular turnover via proliferation and apoptosis. Our study shows that 24-h cytokine treatment with TNFα or IFNγ significantly increased dextran permeability and tight junctional tortuosity, and reduced cellular proliferation. TNFα reduced the percentage of G2/M phase cells, and IFNγ treatment increased cell apoptotic rate. IL-18 did not directly induce significant changes to barrier permeability or cellular turnover. Our study concludes that the inflammatory cytokines, TNFα and IFNγ, directly induce intestinal epithelial barrier dysfunction and alter the tight junctional morphology and rate of cellular turnover in bovine intestinal epithelial cells. |
format | Online Article Text |
id | pubmed-9418144 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-94181442022-08-28 Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier Crawford, Charles K. Lopez Cervantes, Veronica Quilici, Mary L. Armién, Aníbal G. Questa, María Matloob, Muhammad S. Huynh, Leon D. Beltran, Aeelin Karchemskiy, Sophie J. Crakes, Katti R. Kol, Amir Sci Rep Article The small intestinal mucosa constitutes a physical barrier separating the gut lumen from sterile internal tissues. Junctional complexes between cells regulate transport across the barrier, preventing water loss and the entry of noxious molecules or pathogens. Inflammatory diseases in cattle disrupt this barrier; nonetheless, mechanisms of barrier disruption in cattle are poorly understood. We investigated the direct effects of three inflammatory cytokines, TNFα, IFNγ, and IL-18, on the bovine intestinal barrier utilizing intestinal organoids. Flux of fluorescein isothiocyanate (FITC)-labeled dextran was used to investigate barrier permeability. Immunocytochemistry and transmission electron microscopy were used to investigate junctional morphology, specifically tortuosity and length/width, respectively. Immunocytochemistry and flow cytometry was used to investigate cellular turnover via proliferation and apoptosis. Our study shows that 24-h cytokine treatment with TNFα or IFNγ significantly increased dextran permeability and tight junctional tortuosity, and reduced cellular proliferation. TNFα reduced the percentage of G2/M phase cells, and IFNγ treatment increased cell apoptotic rate. IL-18 did not directly induce significant changes to barrier permeability or cellular turnover. Our study concludes that the inflammatory cytokines, TNFα and IFNγ, directly induce intestinal epithelial barrier dysfunction and alter the tight junctional morphology and rate of cellular turnover in bovine intestinal epithelial cells. Nature Publishing Group UK 2022-08-26 /pmc/articles/PMC9418144/ /pubmed/36028741 http://dx.doi.org/10.1038/s41598-022-18771-y Text en © The Author(s) 2022 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 Crawford, Charles K. Lopez Cervantes, Veronica Quilici, Mary L. Armién, Aníbal G. Questa, María Matloob, Muhammad S. Huynh, Leon D. Beltran, Aeelin Karchemskiy, Sophie J. Crakes, Katti R. Kol, Amir Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
title | Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
title_full | Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
title_fullStr | Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
title_full_unstemmed | Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
title_short | Inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
title_sort | inflammatory cytokines directly disrupt the bovine intestinal epithelial barrier |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9418144/ https://www.ncbi.nlm.nih.gov/pubmed/36028741 http://dx.doi.org/10.1038/s41598-022-18771-y |
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