Phospholipase A Subclasses in Acute Respiratory Distress Syndrome
Résumé
Phospholipases A (PLA) catalyse the cleavage of fatty acids esterified at the position of glycerophospholipids. In acute lung injury-acute respiratory distress syndrome (ALI-ARDS) several distinct isoenzymes appear in lung cells and fluid. Some are capable to trigger molecular events leading to enhanced inflammation and lung damage and others have a role in lung surfactant recycling preserving lung function: Secreted forms (groups sPLA-IIA, -V, -X) can directly hydrolyze surfactant phospholipids. Cytosolic PLA (cPLA-IVA) requiring Ca has a preference for arachidonate, the precursor of eicosanoids which participate in the inflammatory response in the lung. Ca-independent intracellular PLAs (iPLA) take part in surfactant phospholipids turnover within alveolar cells. Acidic Ca-independent PLA (aiPLA), of lysosomal origin, has additionally antioxidant properties, (peroxiredoxin VI activity), and participates in the formation of dipalmitoyl-phosphatidylcholine in lung surfactant. PAF-AH degrades PAF, a potent mediator of inflammation, and oxidatively fragmented phospholipids but also leads to toxic metabolites. Therefore, the regulation of PLA isoforms could be a valuable approach for ARDS treatment.
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