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Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal

Helicobacter pylori (HP) infection is one of the most frequent bacterial infections in humans and is associated with the pathogenesis of gastric motility disorders such as delayed gastric emptying (DGE). Although HP infection is considered to delay gastric emptying, there has been little research on...

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Autores principales: Liu, Bin, Dong, Jun, Wang, Shasha, Yu, Haining, Li, Zhongchao, Sun, Pengfei, Zhao, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8111862/
https://www.ncbi.nlm.nih.gov/pubmed/33986828
http://dx.doi.org/10.3892/etm.2021.10095
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author Liu, Bin
Dong, Jun
Wang, Shasha
Yu, Haining
Li, Zhongchao
Sun, Pengfei
Zhao, Lei
author_facet Liu, Bin
Dong, Jun
Wang, Shasha
Yu, Haining
Li, Zhongchao
Sun, Pengfei
Zhao, Lei
author_sort Liu, Bin
collection PubMed
description Helicobacter pylori (HP) infection is one of the most frequent bacterial infections in humans and is associated with the pathogenesis of gastric motility disorders such as delayed gastric emptying (DGE). Although HP infection is considered to delay gastric emptying, there has been little research on the underlying mechanism. Gastric motility involves interactions among gastrointestinal hormones, smooth muscle, enteric and extrinsic autonomic nerves and interstitial cells of Cajal (ICCs), and ICCs play an important role in gastrointestinal motility. Mutation or loss of stem cell factor (SCF) expression is known to reduce the number of ICCs or alter the integrity of the ICC network, contributing to gastrointestinal dysmotility. The aim of the present study was to investigate whether a reduction in ICCs contributes to the DGE caused by HP. A mouse model of HP infection was established and gastric emptying was compared between HP-infected and uninfected mice using the bead method. In addition, ICC counts and SCF expression levels in gastric tissue were evaluated using immunohistochemistry and western blotting, respectively. The results revealed that gastric emptying was significantly slower, the number of ICCs in gastric tissue was significantly reduced and the protein level of SCF in gastric tissue was significantly decreased in HP-infected mice compared with uninfected mice. Therefore, it may be concluded that HP reduced the number of ICCs by decreasing the expression of SCF protein in gastric tissue, thereby causing DGE.
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spelling pubmed-81118622021-05-12 Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal Liu, Bin Dong, Jun Wang, Shasha Yu, Haining Li, Zhongchao Sun, Pengfei Zhao, Lei Exp Ther Med Articles Helicobacter pylori (HP) infection is one of the most frequent bacterial infections in humans and is associated with the pathogenesis of gastric motility disorders such as delayed gastric emptying (DGE). Although HP infection is considered to delay gastric emptying, there has been little research on the underlying mechanism. Gastric motility involves interactions among gastrointestinal hormones, smooth muscle, enteric and extrinsic autonomic nerves and interstitial cells of Cajal (ICCs), and ICCs play an important role in gastrointestinal motility. Mutation or loss of stem cell factor (SCF) expression is known to reduce the number of ICCs or alter the integrity of the ICC network, contributing to gastrointestinal dysmotility. The aim of the present study was to investigate whether a reduction in ICCs contributes to the DGE caused by HP. A mouse model of HP infection was established and gastric emptying was compared between HP-infected and uninfected mice using the bead method. In addition, ICC counts and SCF expression levels in gastric tissue were evaluated using immunohistochemistry and western blotting, respectively. The results revealed that gastric emptying was significantly slower, the number of ICCs in gastric tissue was significantly reduced and the protein level of SCF in gastric tissue was significantly decreased in HP-infected mice compared with uninfected mice. Therefore, it may be concluded that HP reduced the number of ICCs by decreasing the expression of SCF protein in gastric tissue, thereby causing DGE. D.A. Spandidos 2021-07 2021-04-22 /pmc/articles/PMC8111862/ /pubmed/33986828 http://dx.doi.org/10.3892/etm.2021.10095 Text en Copyright: © Liu et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Bin
Dong, Jun
Wang, Shasha
Yu, Haining
Li, Zhongchao
Sun, Pengfei
Zhao, Lei
Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal
title Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal
title_full Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal
title_fullStr Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal
title_full_unstemmed Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal
title_short Helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of Cajal
title_sort helicobacter pylori causes delayed gastric emptying by decreasing interstitial cells of cajal
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8111862/
https://www.ncbi.nlm.nih.gov/pubmed/33986828
http://dx.doi.org/10.3892/etm.2021.10095
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