FC-GAMMA-RII, FC-GAMMA-RIII, AND CD18 RECEPTORS MEDIATE IN PART NEUTROPHIL ACTIVATION ON A PLASMA COATED EXPANDED POLYTETRAFLUOROETHYLENE SURFACE

Background. A biomaterial-induced polymorhonuclear neutrophil (PMN) de fect may predispose the implanted vascular graft to infection. PMNs bi nd, activate, and undergo morphologic changes when exposed to uncoated or plasma coated expanded polytetrafluoroethylene (ePTFE) surfaces. T he purpose of this study was to investigate whether the CD18 integrin receptor or the immunoglobulin receptors FcyRII and FcyRIII mediate ei ther PMN binding or activation on epTFE. Methods. PMN binding and acti vation were determined after incubation of these cells on human immuno globulin (IgG) or fibrinogen coated surfaces and uncoated or plasma co ated ePTFE. PMN activation was measured by using the ferricytochrome r eduction assay. Binding was determined with chromium 51-labeled PMNs. To block the FryRII, FcyRIII, and CD18 receptors, PMNs were preincubat ed with the monoclonal antibodies (mAbs) IV.3 3G8, and IB4, respective ly. Irrelevant isotype matched mAbs were used as control. Results. Mon oclonal antibody IB4 inhibited binding of activated PMNs to fibrinogen coated surfaces. Binding to IgG was affected by either mAb IB4 or IV. 3 but the greatest degree of inhibition was achieved when mAbs IB4 and IV.3 were used in combination. IgG-induced activation was partially i nhibited by mAb IV.3 but was fully inhibited by a combination of mAbs IB4 and IV.3 The mAbs did not affect PMN binding to uncoated or plasma coated ePTFE nor was PMN activation on the uncoated ePTFE surface inh ibited. PMN activation on the plasma coated ePTFE surface was, however , partially inhibited by the combination of mAb IB4 with either mAb IV .3 or 3G8. Conclusions. A synergistic interaction between the PMN FcyR II receptor and the CD18 integrin receptor accounts for surface bound IgG-induced cell activation. Both receptors also play a role in mediat ing PMN activation on the plasma-coated ePTFE surface.