Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8302145 | Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids | 2015 | 10 Pages |
Abstract
Overall, our studies suggest that the increased cholesterol-mobilizing activity of sPLA2-HDL and suppression of rise in intracellular Ca2Â + levels are likely mechanism that counteracts agonist-induced activation of neutrophils. These counterintuitive findings imply that neutrophil trafficking and effector responses are altered by sPLA2-HDL during inflammatory conditions.
Keywords
HDLN-formyl-l-methionyl-l-leucyl-l-phenylalaninecomplement component 5aPMNLfMLPC5asPLA2IL-8LPCICAM-1FFAhigh-density lipoproteinSecretory phospholipase A2Free fatty acidInterleukin 8neutrophil extracellular trapsNETphosphatidylcholinepolymorphonuclear leukocytesLysophosphatidylcholinelysophospholipidintracellular adhesion molecule-1neutrophil
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Authors
Sanja Curcic, Michael Holzer, Robert Frei, Lisa Pasterk, Rudolf Schicho, Akos Heinemann, Gunther Marsche,