Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Sep 28, 2009; 15(36): 4491-4498
Published online Sep 28, 2009. doi: 10.3748/wjg.15.4491
Adenosine: An immune modulator of inflammatory bowel diseases
Jeff Huaqing Ye, Vazhaikkurichi M Rajendran
Jeff Huaqing Ye, Digestive Health Center and Southern Tennessee Internal Medicine, Winchester, TN 37398, United States
Vazhaikkurichi M Rajendran, Department of Biochemistry and Microbiology, West Virginia University School of Medicine, Morgantown, WV 26506, United States
Author contributions: Ye JH and Rajendran VM both wrote the paper.
Supported by A research grant (DK-018777) from the National Institute of Diabetes and Digestive and Kidney Diseases
Correspondence to: Jeff Huaqing Ye, MD, PhD, Digestive Health Center and Southern Tennessee Internal Medicine, Winchester, Tennessee 37398, United States.
Telephone: +1-931-9623500 Fax: +1-931-9623545
Received: April 10, 2009
Revised: August 25, 2009
Accepted: September 1, 2009
Published online: September 28, 2009

Inflammatory bowel disease (IBD) is a common and lifelong disabling gastrointestinal disease. Emerging treatments are being developed to target inflammatory cytokines which initiate and perpetuate the immune response. Adenosine is an important modulator of inflammation and its anti-inflammatory effects have been well established in humans as well as in animal models. High extracellular adenosine suppresses and resolves chronic inflammation in IBD models. High extracellular adenosine levels could be achieved by enhanced adenosine absorption and increased de novo synthesis. Increased adenosine concentration leads to activation of the A2a receptor on the cell surface of immune and epithelial cells that would be a potential therapeutic target for chronic intestinal inflammation. Adenosine is transported via concentrative nucleoside transporter and equilibrative nucleoside transporter transporters that are localized in apical and basolateral membranes of intestinal epithelial cells, respectively. Increased extracellular adenosine levels activate the A2a receptor, which would reduce cytokines responsible for chronic inflammation.

Keywords: Crohn’s disease, Ulcerative colitis, Inflammatory bowel diseases, Epithelial cells, Membrane transporters, Immuno-modulator