ArticlePhysiological reports2014
Absence of calcium-independent phospholipase A2 β impairs platelet-activating factor production and inflammatory cell recruitment in Trypanosoma cruzi-infected endothelial cells.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Discovery of Non-Peptidic Compounds against Chagas Disease Applying Pharmacophore Guided Molecular Modelling Approaches.Molecules (Basel, Switzerland) · 2018Article
- Cigarette smoke-induced urothelial cell damage: potential role of platelet-activating factor.Physiological reports · 2017Article
- Mice with Genetic Deletion of Group VIA Phospholipase A2β Exhibit Impaired Macrophage Function and Increased Parasite Load in Trypanosoma cruzi-Induced Myocarditis.Infection and immunity · 2016Article
- Increased susceptibility to bladder inflammation in smokers: targeting the PAF-PAF receptor interaction to manage inflammatory cell recruitment.Physiological reports · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Both acute and chronic phases of Trypanosoma 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 A2 (iPLA2) isoforms iPLA2 β and iPLA2 γ, whereas PAF production was dependent upon iPLA2 β activation alone. Trypanosoma 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 iPLA2 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.
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Registered trials
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