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Mediators of Inflammation
Volume 2012, Article ID 327568, 13 pages
Review Article

Prostaglandin E 𝟐 and the Suppression of Phagocyte Innate Immune Responses in Different Organs

1Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Araraquara, 14801-902 São Paulo, SP, Brazil
2Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo (USP), Av Octávio Pinheiro Brisolla 9-75, Bauru, 17012-901 São Paulo, SP, Brazil
3Department of Microbiology and Immunology, Indiana University School of Medicine, 950 West Walnut Street, Indianapolis, IN 46202, USA

Received 15 February 2012; Revised 19 April 2012; Accepted 3 May 2012

Academic Editor: Ruxana Sadikot

Copyright © 2012 Alexandra Medeiros 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.


The local and systemic production of prostaglandin E2 (PGE2) and its actions in phagocytes lead to immunosuppressive conditions. PGE2 is produced at high levels during inflammation, and its suppressive effects are caused by the ligation of the E prostanoid receptors EP2 and EP4, which results in the production of cyclic AMP. However, PGE2 also exhibits immunostimulatory properties due to binding to EP3, which results in decreased cAMP levels. The various guanine nucleotide-binding proteins (G proteins) that are coupled to the different EP receptors account for the pleiotropic roles of PGE2 in different disease states. Here, we discuss the production of PGE2 and the actions of this prostanoid in phagocytes from different tissues, the relative contribution of PGE2 to the modulation of innate immune responses, and the novel therapeutic opportunities that can be used to control inflammatory responses.