Open AccessAbsence of calcium‐independent phospholipase A 2 β impairs platelet‐activating factor production and inflammatory cell recruitment in T rypanosoma cruzi ‐infected endothelial cells
Author(s) -
Sharma Janhavi,
Eickhoff Christopher S.,
Hoft Daniel F.,
Marentette John O.,
Turk John,
McHowat Jane
Publication year - 2014
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.1002/phy2.196
Subject(s) - trypanosoma cruzi , platelet activating factor , inflammation , endothelium , cell adhesion molecule , arachidonic acid , phospholipase a2 , biology , cell adhesion , tissue factor , phospholipase c , endothelial stem cell , microbiology and biotechnology , platelet , immunology , cell , medicine , in vitro , signal transduction , biochemistry , endocrinology , enzyme , parasite hosting , world wide web , computer science , coagulation
Abstract Both acute and chronic phases of T rypanosoma cruzi ( T . cruzi ) 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 T . cruzi infection. Arachidonic acid release is mediated by activation of the calcium‐independent phospholipase A 2 ( iPLA 2 ) isoforms iPLA 2 β and iPLA 2 γ , whereas PAF production was dependent upon iPLA 2 β activation alone. T rypanosoma cruzi infection also resulted in increased cell surface expression of adhesion molecules. Increased adherence of inflammatory cells to T . cruzi ‐infected endothelium was blocked by inhibition of endothelial cell iPLA 2 β 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.