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首页> 外文期刊>Journal of biomedical materials research. Part B, Applied biomaterials. >Complement activation and inflammation triggered by model biomaterial surfaces.
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Complement activation and inflammation triggered by model biomaterial surfaces.

机译：由模型生物材料表面触发的补体激活和炎症。

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摘要

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.
机译：生物材料介导的补体激活已被反复激活，以作为吞噬细胞反应和炎症的触发因素。然而，尚未建立补体激活与对生物材料表面的炎症反应之间的直接关联。使用动物植入模型和带有各种巯基连接功能的金表面，我们研究了不同表面基团在体外促进补体激活和体内炎症细胞表面介导积累的潜能。在所测试的表面中，巯基甘油和巯基乙醇表面产生最强的炎症反应，这由大量附着的嗜中性粒细胞和单核细胞/巨噬细胞的积累所反映。相反，涂有L-半胱氨酸的表面仅引起较小的炎症反应，而谷胱甘肽修饰的和未处理的金植入物均吸引了最少数量的炎症细胞。巯基甘油表面上炎性细胞的积累似乎是由表面介导的补体激活引起的，因为补体耗竭的动物无法表现出对巯基甘油修饰的植入物的炎症反应。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。至少在这种动物模型中以及在这些模型表面上，我们的结果表明表面介导的补体激活可能是炎症细胞在植入物表面上随后积累的原因。

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