Molecular and cellular mechanisms of tight junction dysfunction in the irritable bowel syndrome

Cheng,Peng; Yao,Jianning; Wang,Chunfeng; Zhang,Lianfeng; Kong,Wuming

doi:10.3892/mmr.2015.3808

Molecular and cellular mechanisms of tight junction dysfunction in the irritable bowel syndrome

Authors:
- Peng Cheng
- Jianning Yao
- Chunfeng Wang
- Lianfeng Zhang
- Wuming Kong
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Affiliations: Department of Gastroenterology, First Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China, Department of Gastroenterology, Affiliated Sixth People's Hospital of Shanghai Jiaotong University, Shanghai 201306, P.R. China
Published online on: May 21, 2015 https://doi.org/10.3892/mmr.2015.3808
Pages: 3257-3264
Copyright: © Cheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

The pathophysiological mechanisms of the irritable bowel syndrome (IBS), one of the most prevalent gastrointestinal disorders, are complex and have not been fully elucidated. The present study aimed to investigate the molecular and cellular mechanisms of tight junction (TJ) dysfunction in IBS. Intestinal tissues of IBS and non‑IBS patients were examined to observe cellular changes by cell chemical tracer electron microscopy and transmission electron microscopy, and intestinal claudin‑1 protein was detected by immunohistochemistry, western blot analysis and fluorescence quantitative polymerase chain reaction. Compared with the control group, TJ broadening and the tracer extravasation phenomenon were observed in the diarrhea‑predominant IBS group, and a greater number of neuroendocrine cells and mast cells filled with high‑density particles in the endocrine package pulp as well as a certain extent of vacuolization were present. The expression of claudin‑1 in diarrhea‑predominant IBS patients was decreased, while it was increased in constipation‑predominant IBS patients. In conclusion, the results of the present study indicated that changes in cellular structure and claudin‑1 levels were associated with Tjs in IBS.

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