Phospholipase A in acute lung injury after trauma and sepsis: its relation to the inflammatory mediators PMN-elastase, C3a, and neopterin.

Inflammatory mediators involved in the pathogenesis of the adult respiratory distress syndrome (ARDS) are products of the humeral cascade systems like the complement cascade and substances released from neutrophil granulocytes and macrophages like proteases, O2-radicals and arachidonate products. Phospholipase A2 (PLA) was shown by Vadas et al. to be correlated with circulatory shock in the sepsis syndrome, the probably most important underlying disease of ARDS. In a clinical study in 48 patients at risk for ARDS after trauma and sepsis we found plasma PLA elevated (52 +/- 5 U/l) in sepsis, with a positive correlation to the complement split product C3a (r = 0.42, p less than 0.01) and neopterin (r = 0.49, p less than 0.05), which serves as a marker of macrophage stimulation. Elastase-alpha 1PI and C3a showed higher plasma levels in patients with ARDS compared with non-ARDS patients, whereas the neopterin and PLA concentrations were not different with regard to ARDS. The relation between PLA and neopterin shown in the study is consistent with the possibility of macrophages being a source of the plasma PLA, as reported in experimental studies.