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Phospholipase A2 (PLA2), an enzyme protein that catalyzes the hydrolysis of phospholipids at the sn-2 position to generate lysophospholipids and free fatty acids, has been implicated to play a critical role in the pathogenesis of inflammatory disorders including shock and sepsis. In sepsis patients, plasma PLA2 activity was increased and the increased circulating PLA2 correlated positively with severity of organ dysfunction and the eventual mortality. In human volunteers, endotoxin challenge activated serum PLA2 and elicited many features of sepsis syndrome. In laboratory animals, secretory PLA2 (sPLA2) and cytosolic PLA2 (cPLA2) activities were increased in plasma and various organs including liver, heart, lung, spleen, thymus, and aorta following endotoxin administration and the increased plasma sPLA2 was proportional to the decrease in the mean arterial blood pressure. The notion that PLA2 plays an important role in the pathogenesis of sepsis and septic shock is further supported by recent finding that treatment of sepsis animals with antisense oligonucleotides targeting sPLA2 and cPLA2, in conjunction with antibiotics, decreased sPLA2 and cPLA2 protein expression in major organs, and the decreased tissue PLA2 protein expression in multiple organs was accompanied by an absolute reduction of 30.8 % in 35-day mortality, in rats with sepsis.
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