McNally A K, Anderson J M
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106.
Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):10119-23. doi: 10.1073/pnas.91.21.10119.
As part of an ongoing investigation into the role of the monocyte/macrophage in biocompatibility, a major goal is to identify the adhesion mechanisms that initiate and promote the observed in vivo morphologic progression of monocyte-to-macrophage-to-foreign body giant cell on biomaterials. We have exploited differently modified polystyrenes, specific component-depleted sera, and monoclonal antibodies (mAbs) to leukocyte integrins to ask what adhesion mechanisms mediate human blood monocyte adhesion to different surfaces in vitro. Preliminary findings are that monocyte interactions with fluorinated, siliconized, nitrogenated, and oxygenated surfaces are reduced by 50-100% when complement component C3-depleted serum is used for adsorption; reductions vary with material surface properties. Adhesion is restored on all surfaces when C3-depleted serum is replenished with purified C3. Monocyte adhesion to serum-adsorbed surfaces is inhibited by mAbs to the leukocyte integrin beta subunit, CD18 (mAbs 60.3 and MHM23), and partially inhibited by a mAb to the alpha subunit, CD11b (mAb 60.1), suggesting adhesive interactions between adsorbed C3bi (the hemolytically inactive form of the C3b fragment) and the leukocyte integrin CD11b/CD18. However, adsorbed fibrinogen reduces the effectiveness of these mAbs, indicating that alternative adhesion mechanisms may operate depending on the propensities of critical adhesion-mediating components to be adsorbed onto different surfaces.
作为对单核细胞/巨噬细胞在生物相容性中作用的一项正在进行的研究的一部分，一个主要目标是确定引发并促进在生物材料上观察到的单核细胞到巨噬细胞再到异物巨细胞的体内形态学进展的粘附机制。我们利用不同修饰的聚苯乙烯、特定成分缺失的血清以及针对白细胞整合素的单克隆抗体（mAb），来探究在体外介导人血单核细胞粘附到不同表面的粘附机制是什么。初步研究结果表明，当使用补体成分C3缺失的血清进行吸附时，单核细胞与氟化、硅化、氮化和氧化表面的相互作用减少了50% - 100%；减少程度因材料表面性质而异。当用纯化的C3补充C3缺失的血清时，所有表面上的粘附都得以恢复。针对白细胞整合素β亚基CD18的单克隆抗体（mAb 60.3和MHM23）可抑制单核细胞对血清吸附表面的粘附，而针对α亚基CD11b的单克隆抗体（mAb 60.1）则部分抑制这种粘附，这表明吸附的C3bi（C3b片段的无溶血活性形式）与白细胞整合素CD11b/CD18之间存在粘附相互作用。然而，吸附的纤维蛋白原会降低这些单克隆抗体的有效性，这表明取决于关键粘附介导成分吸附到不同表面的倾向，可能存在其他粘附机制。
