Human recombinant platelet phospholipase A2 exacerbates poly-L-arginine induced rat paw edema.

In this study by using the human recombinant non-pancreatic-secreted platelet PLA2 (r-hnps-PLA2) and rabbit polyclonal antibodies directed against either the human (group II) or the porcine enzyme (group I), we have shown a possible involvement of platelet PLA2 in poly-L-arginine (25 kDa)-induced rat paw edema. Local treatment of rats with the anti-platelet-PLA2 antibody (anti-hnps-PLA2) but not with anti-porcine-PLA2 antibody (anti-porc-PLA2) significantly reduced the edema induced by a maximal dose of poly-L-arginine (1 mg/paw). Furthermore when r-hnps-PLA2 (1-10 micrograms) was injected together with a subliminal dose of poly-L-arginine (50 micrograms/paw), a dose-dependent increase in both edema and protein leakage was observed. This effect was selectively inhibited by the anti-hnps-PLA2 (10-100 micrograms/paw) but not anti-porc-PLA2 (10-100 micrograms paw). Thus, platelets seem to be involved in both vascular and cellular components of the inflammatory response by contributing, most likely in the early phase, to the edema formation through secretion of PLA2.