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Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases

Intestinal epithelial cells cover the surface of the intestinal tract. The cells are important for preserving the integrity of the mucosal barriers to protect the host from luminal antigens and pathogens. The mucosal barriers are maintained by the continuous and rapid self-renewal of intestinal epit...

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Detalles Bibliográficos
Autores principales: Ohashi, Wakana, Fukada, Toshiyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6431494/
https://www.ncbi.nlm.nih.gov/pubmed/30984791
http://dx.doi.org/10.1155/2019/8396878
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author Ohashi, Wakana
Fukada, Toshiyuki
author_facet Ohashi, Wakana
Fukada, Toshiyuki
author_sort Ohashi, Wakana
collection PubMed
description Intestinal epithelial cells cover the surface of the intestinal tract. The cells are important for preserving the integrity of the mucosal barriers to protect the host from luminal antigens and pathogens. The mucosal barriers are maintained by the continuous and rapid self-renewal of intestinal epithelial cells. Defects in the self-renewal of these cells are associated with gastrointestinal diseases, including inflammatory bowel diseases and diarrhea. Zinc is an essential trace element for living organisms, and zinc deficiency is closely linked to the impaired mucosal integrity. Recent evidence has shown that zinc transporters contribute to the barrier function of intestinal epithelial cells. In this review, we describe the recent advances in understanding the role of zinc and zinc transporters in the barrier function and homeostasis of intestinal epithelial cells.
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spelling pubmed-64314942019-04-14 Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases Ohashi, Wakana Fukada, Toshiyuki J Immunol Res Review Article Intestinal epithelial cells cover the surface of the intestinal tract. The cells are important for preserving the integrity of the mucosal barriers to protect the host from luminal antigens and pathogens. The mucosal barriers are maintained by the continuous and rapid self-renewal of intestinal epithelial cells. Defects in the self-renewal of these cells are associated with gastrointestinal diseases, including inflammatory bowel diseases and diarrhea. Zinc is an essential trace element for living organisms, and zinc deficiency is closely linked to the impaired mucosal integrity. Recent evidence has shown that zinc transporters contribute to the barrier function of intestinal epithelial cells. In this review, we describe the recent advances in understanding the role of zinc and zinc transporters in the barrier function and homeostasis of intestinal epithelial cells. Hindawi 2019-03-10 /pmc/articles/PMC6431494/ /pubmed/30984791 http://dx.doi.org/10.1155/2019/8396878 Text en Copyright © 2019 Wakana Ohashi and Toshiyuki Fukada. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Ohashi, Wakana
Fukada, Toshiyuki
Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases
title Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases
title_full Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases
title_fullStr Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases
title_full_unstemmed Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases
title_short Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases
title_sort contribution of zinc and zinc transporters in the pathogenesis of inflammatory bowel diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6431494/
https://www.ncbi.nlm.nih.gov/pubmed/30984791
http://dx.doi.org/10.1155/2019/8396878
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