Katz D A, Haimovich B, Greco R S
Department of Surgery, UMD-NJ-Robert Wood Johnson Medical School, New Brunswick 08903, USA.
Surgery. 1995 Aug;118(2):154-60; discussion 160-1. doi: 10.1016/s0039-6060(05)80318-6.
A biomaterial-induced polymorphonuclear neutrophil (PMN) defect may predispose the implanted vascular graft to infection. PMNs bind, activate, and undergo morphologic changes when exposed to uncoated or plasma coated expanded polytetrafluoroethylene (ePTFE) surfaces. The purpose of this study was to investigate whether the CD18 integrin receptor or the immunoglobulin receptors Fc gamma RII and Fc gamma RIII mediate either PMN binding or activation on ePTFE.
PMN binding and activation were determined after incubation of these cells on human immunoglobulin (IgG) or fibrinogen coated surfaces and uncoated or plasma coated ePTFE. PMN activation was measured by using the ferricytochrome reduction assay. Binding was determined with chromium 51-labeled PMNs. To block the Fc gamma RII, Fc gamma RIII, and CD18 receptors, PMNs were preincubated with the monoclonal antibodies (mAbs) IV.3, 3G8, and IB4, respectively. Irrelevant isotype matched mAbs were used as control.
Monoclonal 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 inhibited 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 inhibited. 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.
A synergistic interaction between the PMN Fc gamma RII receptor and the CD18 integrin receptor accounts for surface bound IgG-induced cell activation. Both receptors also play a role in mediating PMN activation on the plasma-coated ePTFE surface.
生物材料诱导的多形核中性粒细胞(PMN)缺陷可能使植入的血管移植物易于感染。当暴露于未涂层或血浆涂层的膨体聚四氟乙烯(ePTFE)表面时,PMN会结合、激活并发生形态变化。本研究的目的是调查CD18整合素受体或免疫球蛋白受体FcγRII和FcγRIII是否介导PMN在ePTFE上的结合或激活。
将这些细胞在人免疫球蛋白(IgG)或纤维蛋白原包被的表面以及未涂层或血浆涂层的ePTFE上孵育后,测定PMN的结合和激活情况。通过铁细胞色素还原试验测量PMN的激活。用铬51标记的PMN测定结合情况。为了阻断FcγRII、FcγRIII和CD18受体,分别用单克隆抗体(mAb)IV.3、3G8和IB4对PMN进行预孵育。无关的同型匹配mAb用作对照。
单克隆抗体IB4抑制活化的PMN与纤维蛋白原包被表面的结合。与IgG的结合受mAb IB4或IV.3影响,但当mAb IB4和IV.3联合使用时抑制程度最大。IgG诱导的激活被mAb IV.3部分抑制,但被mAb IB4和IV.3联合使用完全抑制。这些mAb不影响PMN与未涂层或血浆涂层ePTFE的结合,也不抑制未涂层ePTFE表面上的PMN激活。然而,mAb IB4与mAb IV.3或3G8联合使用可部分抑制血浆涂层ePTFE表面上的PMN激活。
PMN FcγRII受体与CD18整合素受体之间的协同相互作用导致表面结合的IgG诱导细胞激活。这两种受体在介导血浆涂层ePTFE表面上的PMN激活中也起作用。