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Originally published In Press as doi:10.1074/jbc.M201803200 on April 29, 2002

J. Biol. Chem., Vol. 277, Issue 29, 26012-26020, July 19, 2002
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Indomethacin Causes Prostaglandin D2-like and Eotaxin-like Selective Responses in Eosinophils and Basophils*

Victoria E. L. StubbsDagger , Petra Schratl§, Adele HartnellDagger , Timothy J. WilliamsDagger , Bernhard A. Peskar§, Akos Heinemann§||, and Ian SabroeDagger **

From the Dagger  Leukocyte Biology Section, Biomedical Sciences Division, Imperial College Faculty of Medicine, Imperial College of Science, Technology and Medicine, South Kensington, London SW7 2AZ, United Kingdom and the § Department of Experimental and Clinical Pharmacology, Universitatsplatz 4, Graz A-8010, Austria

We investigated the actions of a panel of nonsteroidal anti-inflammatory drugs on eosinophils, basophils, neutrophils, and monocytes. Indomethacin alone was a potent and selective inducer of eosinophil and basophil shape change. In eosinophils, indomethacin induced chemotaxis, CD11b up-regulation, respiratory burst, and L-selectin shedding but did not cause up-regulation of CD63 expression. Pretreatment of eosinophils with indomethacin also enhanced subsequent eosinophil shape change induced by eotaxin, although treatment with higher concentrations of indomethacin resulted in a decrease in the expression of the major eosinophil chemokine receptor, CCR3. Indomethacin activities and cell selectivity closely resembled those of prostaglandin D2 (PGD2). Eosinophil shape change in response to eotaxin was inhibited by pertussis toxin, but indomethacin- and PGD2-induced shape change responses were not. Treatment of eosinophils with specific inhibitors of phospholipase C (U-73122), phosphatidylinositol 3-kinase (LY-294002), and p38 mitogen-activated protein kinase (SB-202190) revealed roles for these pathways in indomethacin signaling. Indomethacin and its analogues may therefore provide a structural basis from which selective PGD2 receptor small molecule antagonists may be designed and which may have utility in the treatment of allergic inflammatory disease.

* This work was supported by National Asthma Campaign Project Grant 99/012 (to V. E. L. S.), a grant from the Medical Research Council UK (to I. S.), a grant from the Wellcome Trust (to A. Hartnell and T. J. W.), a grant from the National Asthma Campaign (to T. J. W.), a grant from the Royal Society (to T. J. W. and B. A. P.), and Austrian Science Fund FWF Grant P15453 (to A. Heinemann).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These two authors contributed equally to this work as principal investigators.

|| To whom correspondence should be addressed: Dept. of Experimental and Clinical Pharmacology, Universitatsplatz 4, A-8010 Graz, Austria. E-mail: akos.heinemann@kfunigraz.ac.at.

** Present address: Division of Genomic Medicine, University of Sheffield, M Floor, Royal Hallamshire Hospital, Sheffield S10 2JF, United Kingdom.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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