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Mediators of Inflammation
Volume 2015, Article ID 427125, 8 pages
Review Article

Pathophysiological Role of Extracellular Purinergic Mediators in the Control of Intestinal Inflammation

Yosuke Kurashima,1,2,3 Hiroshi Kiyono,2,3,4 and Jun Kunisawa1,2,4,5,6

1Laboratory of Vaccine Materials, National Institute of Biomedical Innovation, Osaka 567-0085, Japan
2Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
3Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo 102-0075, Japan
4International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
5Department of Microbiology and Immunology, Kobe University School of Medicine, Kobe 650-0017, Japan
6Graduate School of Pharmaceutical Sciences and Graduate School of Dentistry, Osaka University, Osaka 565-0871, Japan

Received 5 August 2014; Accepted 30 September 2014

Academic Editor: Ishak O. Tekin

Copyright © 2015 Yosuke Kurashima et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purinergic mediators such as adenosine 5′-triphosphate (ATP) are released into the extracellular compartment from damaged tissues and activated immune cells. They are then recognized by multiple purinergic P2X and P2Y receptors. Release and recognition of extracellular ATP are associated with both the development and the resolution of inflammation and infection. Accumulating evidence has recently suggested the potential of purinergic receptors as novel targets for drugs for treating intestinal disorders, including intestinal inflammation and irritable bowel syndrome. In this review, we highlight recent findings regarding the pathophysiological role of purinergic mediators in the development of intestinal inflammation.