Relationship between intestinal microbiota and ulcerative colitis: Mechanisms and clinical application of probiotics and fecal microbiota transplantation

Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal...

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Published inWorld journal of gastroenterology : WJG Vol. 24; no. 1; pp. 5 - 14
Main Authors Shen, Zhao-Hua, Zhu, Chang-Xin, Quan, Yong-Sheng, Yang, Zhen-Yu, Wu, Shuai, Luo, Wei-Wei, Tan, Bei, Wang, Xiao-Yan
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Inc 07.01.2018
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Abstract Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation (FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in the pathogenesis and treatment of UC.
AbstractList Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation (FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in the pathogenesis and treatment of UC.Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation (FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in the pathogenesis and treatment of UC.
Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation (FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in the pathogenesis and treatment of UC.
Author Shen, Zhao-Hua
Wang, Xiao-Yan
Quan, Yong-Sheng
Luo, Wei-Wei
Yang, Zhen-Yu
Zhu, Chang-Xin
Wu, Shuai
Tan, Bei
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– sequence: 3
  givenname: Yong-Sheng
  surname: Quan
  fullname: Quan, Yong-Sheng
– sequence: 4
  givenname: Zhen-Yu
  surname: Yang
  fullname: Yang, Zhen-Yu
– sequence: 5
  givenname: Shuai
  surname: Wu
  fullname: Wu, Shuai
– sequence: 6
  givenname: Wei-Wei
  surname: Luo
  fullname: Luo, Wei-Wei
– sequence: 7
  givenname: Bei
  surname: Tan
  fullname: Tan, Bei
– sequence: 8
  givenname: Xiao-Yan
  surname: Wang
  fullname: Wang, Xiao-Yan
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29358877$$D View this record in MEDLINE/PubMed
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Keywords Probiotics
Clinical application
Fecal microbiota transplantation
Intestinal microbiota
Mechanism
Ulcerative colitis
Language English
License This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
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Correspondence to: Xiao-Yan Wang, MD, PhD, Professor, Department of Gastroenterology, Third Xiangya Hospital, Central South University, 138 Tongzipo Road, Yuelu District, Changsha 410013, Hunan Province, China. wangxiaoyan2913@126.com
Author contributions: Shen ZH wrote the manuscript; Wang XY contributed to the manuscript critical revision; all authors approved the final version of the article.
Telephone: +86-13974889301 Fax: +86-731-88618457
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Snippet Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders,...
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SubjectTerms Animals
Bacteria - growth & development
Bacteria - immunology
Colitis, Ulcerative - diagnosis
Colitis, Ulcerative - immunology
Colitis, Ulcerative - microbiology
Colitis, Ulcerative - therapy
Colon - immunology
Colon - microbiology
Fecal Microbiota Transplantation - adverse effects
Gastrointestinal Microbiome
Host-Pathogen Interactions
Humans
Probiotics - adverse effects
Probiotics - therapeutic use
Review
Treatment Outcome
Title Relationship between intestinal microbiota and ulcerative colitis: Mechanisms and clinical application of probiotics and fecal microbiota transplantation
URI https://www.ncbi.nlm.nih.gov/pubmed/29358877
https://www.proquest.com/docview/1990489081
https://pubmed.ncbi.nlm.nih.gov/PMC5757125
Volume 24
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