Public Release:  A future strategy for the treatment of patients with ulcerative colitis

World Journal of Gastroenterology

Ulcerative colitis (UC) is characterized by frequent diarrheal attacks and anal bleeding. Histologic characteristics of UC are the invasion of the crypt epithelium and lamina propria by peripheral blood mononuclear cells (PBMCs), disruption of the epithelial lining, and consequently mucosal ulceration and crypt abscess formation in the bowel wall. Regulation of the migration of inflammatory leukocytes into the intestinal tissues is considered to be a therapeutic option for patients with UC. Chemokine stromal cell-derived factor-1 receptor (CXCR4) is specific receptor for chemokine chemokine stromal cell-derived factor-1 (CXCL12), and the latter is a potent chemoattractant for PBMCs. The expression of CXCL12 and CXCR4 on intestinal epithelial cells, lamina propria T cells and PBMCs are significantly increased in UC patients, and block of CXCR4 ameliorates the colonic inflammation in experimental colitis. Whether a CXCR4 antagonist enhances epithelial barrier function, however, has not been unequivocally addressed.

A research article to be published on June 21, 2010 in the World Journal of Gastroenterology addresses this question. This is the first study to report that, in addition to inflammation inhibition, the CXCR4 antagonist, AMD3100, also decreased epithelial apoptosis and gut permeability in experimental colitis, and consequently enhanced the epithelial barrier function.

Their results suggested a pivotal role of the CXCL12/CXCR4 chemokine axis in the pathogenesis of UC. By understanding the role of CXCR4 in colonic inflammation and epithelial barrier, this study may represent a future strategy for therapeutic intervention in the treatment of patients with UC.

###

Reference: Xia XM, Wang FY, Xu WA, Wang ZK, Liu J, Lu YK, Jin XX, Lu H, Shen YZ. CXCR4 antagonist AMD3100 attenuates colonic damage in mice with experimental colitis. World J Gastroenterol 2010; 16(23): 2873-2880

http://www.wjgnet.com/1007-9327/full/v16/i23/2873.htm

Correspondence to: Fang-Yu Wang, Professor, Department of Gastroenterology and Hepatology, Jinling Hospital, 305 Zhongshan East Road, Nanjing 210002, Jiangsu Province, China. wangfy65@gmail.com

Telephone: +86-25-80860051 Fax: +86-25-80860151

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2009 IF: 2.092. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.