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Enteric microbiota leads to new therapeutic strategies for ulcerative colitis.
World J Gastroenterol 2014; 20(42):15657-63WJ

Abstract

Ulcerative colitis (UC) is a leading form of inflammatory bowel disease that involves chronic relapsing or progressive inflammation. As a significant proportion of UC patients treated with conventional therapies do not achieve remission, there is a pressing need for the development of more effective therapies. The human gut contains a large, diverse, and dynamic population of microorganisms, collectively referred to as the enteric microbiota. There is a symbiotic relationship between the human host and the enteric microbiota, which provides nutrition, protection against pathogenic organisms, and promotes immune homeostasis. An imbalance of the normal enteric microbiota composition (termed dysbiosis) underlies the pathogenesis of UC. A reduction of enteric microbiota diversity has been observed in UC patients, mainly affecting the butyrate-producing bacteria, such as Faecalibacterium prausnitzii, which can repress pro-inflammatory cytokines. Many studies have shown that enteric microbiota plays an important role in anti-inflammatory and immunoregulatory activities, which can benefit UC patients. Therefore, manipulation of the dysbiosis is an attractive approach for UC therapy. Various therapies targeting a restoration of the enteric microbiota have shown efficacy in treating patients with active and chronic forms of UC. Such therapies include fecal microbiota transplantation, probiotics, prebiotics, antibiotics, helminth therapy, and dietary polyphenols, all of which can alter the abundance and composition of the enteric microbiota. Although there have been many large, randomized controlled clinical trials assessing these treatments, the effectiveness and safety of these bacteria-driven therapies need further evaluation. This review focuses on the important role that the enteric microbiota plays in maintaining intestinal homeostasis and discusses new therapeutic strategies targeting the enteric microbiota for UC.

Authors+Show Affiliations

Wei-Xu Chen, Li-Hua Ren, Rui-Hua Shi, Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China.Wei-Xu Chen, Li-Hua Ren, Rui-Hua Shi, Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China.Wei-Xu Chen, Li-Hua Ren, Rui-Hua Shi, Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

25400449

Citation

Chen, Wei-Xu, et al. "Enteric Microbiota Leads to New Therapeutic Strategies for Ulcerative Colitis." World Journal of Gastroenterology, vol. 20, no. 42, 2014, pp. 15657-63.
Chen WX, Ren LH, Shi RH. Enteric microbiota leads to new therapeutic strategies for ulcerative colitis. World J Gastroenterol. 2014;20(42):15657-63.
Chen, W. X., Ren, L. H., & Shi, R. H. (2014). Enteric microbiota leads to new therapeutic strategies for ulcerative colitis. World Journal of Gastroenterology, 20(42), pp. 15657-63. doi:10.3748/wjg.v20.i42.15657.
Chen WX, Ren LH, Shi RH. Enteric Microbiota Leads to New Therapeutic Strategies for Ulcerative Colitis. World J Gastroenterol. 2014 Nov 14;20(42):15657-63. PubMed PMID: 25400449.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enteric microbiota leads to new therapeutic strategies for ulcerative colitis. AU - Chen,Wei-Xu, AU - Ren,Li-Hua, AU - Shi,Rui-Hua, PY - 2014/02/25/received PY - 2014/05/11/revised PY - 2014/06/26/accepted PY - 2014/11/18/entrez PY - 2014/11/18/pubmed PY - 2015/8/19/medline KW - Dysbiosis KW - Enteric microbiota KW - Fecal microbiota transplantation KW - Polyphenol KW - Probiotic KW - Ulcerative colitis SP - 15657 EP - 63 JF - World journal of gastroenterology JO - World J. Gastroenterol. VL - 20 IS - 42 N2 - Ulcerative colitis (UC) is a leading form of inflammatory bowel disease that involves chronic relapsing or progressive inflammation. As a significant proportion of UC patients treated with conventional therapies do not achieve remission, there is a pressing need for the development of more effective therapies. The human gut contains a large, diverse, and dynamic population of microorganisms, collectively referred to as the enteric microbiota. There is a symbiotic relationship between the human host and the enteric microbiota, which provides nutrition, protection against pathogenic organisms, and promotes immune homeostasis. An imbalance of the normal enteric microbiota composition (termed dysbiosis) underlies the pathogenesis of UC. A reduction of enteric microbiota diversity has been observed in UC patients, mainly affecting the butyrate-producing bacteria, such as Faecalibacterium prausnitzii, which can repress pro-inflammatory cytokines. Many studies have shown that enteric microbiota plays an important role in anti-inflammatory and immunoregulatory activities, which can benefit UC patients. Therefore, manipulation of the dysbiosis is an attractive approach for UC therapy. Various therapies targeting a restoration of the enteric microbiota have shown efficacy in treating patients with active and chronic forms of UC. Such therapies include fecal microbiota transplantation, probiotics, prebiotics, antibiotics, helminth therapy, and dietary polyphenols, all of which can alter the abundance and composition of the enteric microbiota. Although there have been many large, randomized controlled clinical trials assessing these treatments, the effectiveness and safety of these bacteria-driven therapies need further evaluation. This review focuses on the important role that the enteric microbiota plays in maintaining intestinal homeostasis and discusses new therapeutic strategies targeting the enteric microbiota for UC. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/25400449/Enteric_microbiota_leads_to_new_therapeutic_strategies_for_ulcerative_colitis_ L2 - http://www.wjgnet.com/1007-9327/full/v20/i42/15657.htm DB - PRIME DP - Unbound Medicine ER -