Absence of calcium‐independent phospholipase A2β impairs platelet‐activating factor production and inflammatory cell recruitment in Trypanosoma cruzi‐infected endothelial cells. Issue 1 (6th January 2014)

• Record Type: Journal Article
• Authors: Sharma, Janhavi; Eickhoff, Christopher S.; Hoft, Daniel F.; Marentette, John O.; Turk, John; McHowat, Jane
• Is Part Of: Physiological reports. Volume 2:Issue 1(2014:Jan.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2014-01-06
• Subjects: Physiology -- Periodicals; 571
• DOI: 10.1002/phy2.196
• Languages: English
• ISSNs: 2051-817X

Abstract

<abstract abstract-type="main" id="phy2196-abs-0001"> <title>Abstract</title> <p>Both acute and chronic phases of <italic>Trypanosoma cruzi</italic> (<italic>T. cruzi</italic>) infection are characterized by tissue inflammation, mainly in the heart. A key step in the inflammatory process is the transmigration of inflammatory cells across the endothelium to underlying infected tissues. We observed increased arachidonic acid release and platelet‐activating factor (PAF) production in human coronary artery endothelial cells (HCAEC) at up to 96 h of <italic>T. cruzi</italic> infection. Arachidonic acid release is mediated by activation of the calcium‐independent phospholipase A₂ (iPLA₂) isoforms iPLA₂<italic>β</italic> and iPLA₂<italic>γ</italic>, whereas PAF production was dependent upon iPLA₂<italic>β</italic> activation alone. <italic>Trypanosoma cruzi</italic> infection also resulted in increased cell surface expression of adhesion molecules. Increased adherence of inflammatory cells to <italic>T. cruzi</italic>‐infected endothelium was blocked by inhibition of endothelial cell iPLA₂<italic>β</italic> or by blocking the PAF receptor on inflammatory cells. This suggests that PAF, in combination with adhesion molecules, might contribute to parasite clearing in the heart by recruiting inflammatory cells to the endothelium.</p> </abstract>