Tang L, Liu L, Elwing H B
Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
J Biomed Mater Res. 1998 Aug;41(2):333-40. doi: 10.1002/(sici)1097-4636(199808)41:2<333::aid-jbm19>3.0.co;2-l.
Biomaterial-mediated complement activation repeatedly has been invoked as a trigger of phagocyte reactions and inflammation. However, a direct correlation between complement activation and inflammatory responses to biomaterial surfaces has yet to be established. Using an animal implantation model and gold surfaces bearing various thiol-linked functionalities, we investigated the potency of different surface groups in prompting complement activation in vitro and surface-mediated accumulation of inflammatory cells in vivo. Among the surfaces tested, mercaptoglycerol- and mercaptoethanol-bearing surfaces engendered the strongest inflammatory responses, as reflected by the accumulation of large numbers of adherent neutrophils and monocytes/macrophages. In contrast, L-cysteine-coated surfaces caused only minor inflammatory responses, and both glutathione-modified and untreated gold implants attracted minimal numbers of inflammatory cells. The accumulation of inflammatory cells on mercaptoglycerol surfaces appears to arise from surface-mediated complement activation because complement-depleted animals failed to exhibit inflammatory responses to mercaptoglycerol-modified implants. Furthermore, there is a close relationship between surface-mediated complement activation (as measured by in vitro iC3b/C5b-9 generation and C3 deposition) and in vivo inflammatory responses. At least in this animal model and with these model surfaces, our results indicate that surface-mediated complement activation can be responsible for the subsequent accumulation of inflammatory cells on implant surfaces.
生物材料介导的补体激活一再被认为是吞噬细胞反应和炎症的触发因素。然而，补体激活与生物材料表面炎症反应之间的直接关联尚未确立。我们使用动物植入模型和带有各种硫醇连接官能团的金表面，研究了不同表面基团在体外引发补体激活以及在体内引发炎症细胞表面介导积累的能力。在所测试的表面中，带有巯基甘油和巯基乙醇的表面引发了最强的炎症反应，大量黏附的中性粒细胞和单核细胞/巨噬细胞的积累反映了这一点。相比之下，L-半胱氨酸包被的表面仅引起轻微的炎症反应，而谷胱甘肽修饰的和未处理的金植入物吸引的炎症细胞数量极少。巯基甘油表面上炎症细胞的积累似乎源于表面介导的补体激活，因为补体缺陷动物对巯基甘油修饰的植入物未表现出炎症反应。此外，表面介导的补体激活（通过体外iC3b/C5b-9生成和C3沉积测量）与体内炎症反应之间存在密切关系。至少在这个动物模型和这些模型表面中，我们的结果表明表面介导的补体激活可能是植入物表面随后炎症细胞积累的原因。
