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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on June 3, 2005; DOI: 10.1124/jpet.105.085365

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Received for publication March 15, 2005.
Revised June 2, 2005.
Accepted for publication June 2, 2005.

NEUTROPHIL ADHERENCE TO BLADDER MICROVASCULAR ENDOTHELIAL CELLS FOLLOWING PLATELET-ACTIVATING FACTOR ACETYLHYDROLASE INHIBITION

Suzanne M Vinson 1, Alice Rickard 1, Jan S Ryerse 1, Jane McHowat 1*

1 Saint Louis University

* Address correspondence to: E-mail: jane.mchowat{at}tenethealth.com

Abstract

Interstitial cystitis (IC) is an inflammatory bladder condition of unknown etiology. Tryptase released from elevated numbers of activated mast cells is a proposed mediator of the inflammatory process in IC. Previously, we have demonstrated that tryptase increases human bladder microvascular endothelial cell (HBMEC) calcium-independent phospholipase A2 (iPLA2) activity, resulting in the production of multiple biologically active phospholipid metabolites, including platelet-activating factor (PAF), that can mediate inflammation. Since the design of selective PLA2 inhibitors may provide a useful therapeutic strategy to reduce the inflammatory process in IC, we tested several frequently used PLA2 inhibitors on PAF production in tryptase-stimulated HBMEC. Among the inhibitors tested, methyl arachidonyl fluorophosphonate (MAFP) was found to be a potent inhibitor of PAF-acetylhydrolase (PAF-AH) activity. Pretreatment of HBMEC with MAFP significantly increased PAF production in both unstimulated and tryptase-stimulated cells. Additionally, MAFP pretreatment of tryptase-stimulated HBMEC increased both surface expression of P-selectin and polymorphonuclear leukocytes (PMN) adherence to the HMBEC monolayer. These effects suggest that MAFP has a pro-inflammatory effect, irrespective of its ability to inhibit PLA2.


Key words: Bromoenol lactone, PLA2 inhibitors, inflammation, interstitial cystitis, phospholipase A2, selectins


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