HUMAN RECOMBINANT PLATELET PHOSPHOLIPASE A(2) EXACERBATES POLY-L-ARGININE INDUCED RAT PAW EDEMA

In this study by using the human recombinant non-pancreatic-secreted p latelet PLA(2) (r-hnps-PLA(2)) and rabbit polyclonal antibodies direct ed against either the human (group II) or the porcine enzyme (group I) , we have shown a possible involvement of platelet PLA(2) in poly-L-ar ginine (25 kDa)-induced rat paw edema. Local treatment of rats with th e anti-platelet-PLA(2) antibody (anti-hnps-PLA(2)) but not with anti-p orcine-PLA(2) antibody (anti-porc-PLA(2)) significantly reduced the ed ema induced by a maximal dose of poly-L-arginine (1 mg/paw). Furthermo re when r-hnps PLA(2) (1-10 mu g) was injected together with a sublimi nal dose of poly-L-arginine (50 mu g/paw), a dose-dependent increase i n both edema and protein leakage was observed. This effect was selecti vely inhibited by the anti-hnps-PLA(2) (10-100 mu g/paw) but not anti- porc-PLA(2) (10-100 mu g 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 t hrough secretion of PLA(2).