THROMBOTIC THROMBOCYTOPENIC PURPURA PLASMA ENHANCES PLATELET-LEUKOCYTE INTERACTION IN-VITRO

In thrombotic thrombocytopenic purpura (TTP), intravascular platelet a ggregation and formation of platelet-rich thrombi impair the microcirc ulation. TTP plasma has been shown to induce aggregation of normal pla telets in vitro. The present study investigates the formation of activ ated platelet aggregates (aPAg) induced by TTP plasma, with particular attention to their binding to leucocytes (LPAg). Results were compare d with the effects of plasmas from normal controls (CTL) and from pati ents with immune thrombocytopenic purpura (ITP) or thrombosis (THR). F ollowing addition of test plasma to normal whole blood (WB), aPAg and LPAg were assayed by flow cytometry using mAbs against CD41 (platelet marker), CD62p (platelet activation marker) and CD45 (pan-leucocyte ma rker). Compared to control plasma, TTP plasma was more potent than ITP or THR plasma in increasing aPAg; only TTP plasma significantly promo ted leucocyte binding to give increased LPAg. Prior removal of neutrop hils (PMN) from WB by beads coated with anti-CD15 mAB largely prevente d formation of aPAg and LPAg. However, TTP plasma added to normal plat elet-rich plasma significantly increased aPAg, which suggested possibl e hindrance of aPAg formation by erythrocytes and other leucocytes in PMN-depleted blood. We concluded that TTP plasma was most potent in th e induction of aPAg and unique in promoting LPAg formation in WB. Neut rophils, and not other leucocytes, appear to be essential for LPAg for mation. Enhanced PMN-platelet interaction in the microcirculation may facilitate platelet adhesion to vessel walls and promote the formation of platelet-rich microthrombi in TTP.