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Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells
OBJECTIVE: The clostridial triose-phosphate isomerase (tpi) gene is a housekeeping gene that specifically distinguishes Clostridium difficile from other bacteria. This retrospective cohort study was performed to analyze and compare the TPI protein-positive rates in outpatients and hospitalized patie...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6259361/ https://www.ncbi.nlm.nih.gov/pubmed/30392450 http://dx.doi.org/10.1177/0300060518799267 |
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author | Hui, Liangliang Zang, Kui Wang, Min Shang, Futai Zhang, Guoxin |
author_facet | Hui, Liangliang Zang, Kui Wang, Min Shang, Futai Zhang, Guoxin |
author_sort | Hui, Liangliang |
collection | PubMed |
description | OBJECTIVE: The clostridial triose-phosphate isomerase (tpi) gene is a housekeeping gene that specifically distinguishes Clostridium difficile from other bacteria. This retrospective cohort study was performed to analyze and compare the TPI protein-positive rates in outpatients and hospitalized patients with and without diarrhea (control group). METHODS: Western blotting, methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, and flow cytometry were used to investigate the pathogenic mechanism of C. difficile in the development and progression of diarrhea in patients with inflammatory bowel disease (IBD). RESULTS: The TPI protein-positive rates were significantly higher in patients with diarrhea but without IBD than in the healthy control group as well as in patients with diarrhea and IBD than in patients with diarrhea but without IBD. Coculture with C. difficile inhibited aquaporin-1 protein expression in human intestinal microvascular endothelial cells, which significantly reduced the proliferation of these cells and promoted their apoptosis. CONCLUSIONS: Clostridium difficile infection is associated with diarrhea and may be an important risk factor for diarrhea in patients with IBD. Coculture with C. difficile may inhibit the proliferation of intestinal mucosal cells and promote their apoptosis, reduce intestinal aquaporin-1 expression, and inhibit intestinal water uptake. Clostridium difficile is one cause of C. difficile-associated diarrhea. |
format | Online Article Text |
id | pubmed-6259361 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-62593612018-11-30 Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells Hui, Liangliang Zang, Kui Wang, Min Shang, Futai Zhang, Guoxin J Int Med Res Pre-Clinical Research Report OBJECTIVE: The clostridial triose-phosphate isomerase (tpi) gene is a housekeeping gene that specifically distinguishes Clostridium difficile from other bacteria. This retrospective cohort study was performed to analyze and compare the TPI protein-positive rates in outpatients and hospitalized patients with and without diarrhea (control group). METHODS: Western blotting, methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, and flow cytometry were used to investigate the pathogenic mechanism of C. difficile in the development and progression of diarrhea in patients with inflammatory bowel disease (IBD). RESULTS: The TPI protein-positive rates were significantly higher in patients with diarrhea but without IBD than in the healthy control group as well as in patients with diarrhea and IBD than in patients with diarrhea but without IBD. Coculture with C. difficile inhibited aquaporin-1 protein expression in human intestinal microvascular endothelial cells, which significantly reduced the proliferation of these cells and promoted their apoptosis. CONCLUSIONS: Clostridium difficile infection is associated with diarrhea and may be an important risk factor for diarrhea in patients with IBD. Coculture with C. difficile may inhibit the proliferation of intestinal mucosal cells and promote their apoptosis, reduce intestinal aquaporin-1 expression, and inhibit intestinal water uptake. Clostridium difficile is one cause of C. difficile-associated diarrhea. SAGE Publications 2018-11-04 2018-11 /pmc/articles/PMC6259361/ /pubmed/30392450 http://dx.doi.org/10.1177/0300060518799267 Text en © The Author(s) 2018 http://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Pre-Clinical Research Report Hui, Liangliang Zang, Kui Wang, Min Shang, Futai Zhang, Guoxin Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
title | Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
title_full | Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
title_fullStr | Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
title_full_unstemmed | Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
title_short | Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
title_sort | coculture with clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells |
topic | Pre-Clinical Research Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6259361/ https://www.ncbi.nlm.nih.gov/pubmed/30392450 http://dx.doi.org/10.1177/0300060518799267 |
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