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Toll-like Receptor 2-mediated Inflammatory Response to Polymeric Biomaterials

机译:Toll样受体2介导的聚合物生物材料介导的炎症反应

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These data shows that: (1) lysate-derived DAMPs competed with serum proteins for biomaterial surface interactions in vitro; (2) lysate-derived DAMPs adsorbed to polymer surfaces potently NF-kB transcription factors, to a greater extent than serum protein; (3) DAMP-adsorbed polymer surfaces activated NF-kB primarily through TLR2; and (4) exposure of RAW-Blue macrophages to DAMP-adsorbed surfaces strongly induced the production of pro-inflammatory cytokines IL-6 and TNF-a in a TLR2-dependent manner. These results suggest that DAMPs, in their adsorbed conformation, are capable of inducing a potent pro-inflammatory response in macrophages through TLRs, and that TLR signaling pathways should be investigated further as potential therapeutic targets for modulating host responses to implanted biomaterials.
机译:这些数据表明:(1)裂解物衍生的潮湿,用血清蛋白质竞争,用于体外生物材料表面相互作用; (2)裂解物衍生的潮湿吸附到聚合物表面易于NF-KB转录因子,在血清蛋白的程度上更大程度; (3)湿吸附的聚合物表面主要通过TLR2激活NF-Kb; (4)暴露于湿吸附的表面的原始蓝色巨噬细胞强烈诱导诸如TLR2依赖性方式的促炎细胞因子IL-6和TNF-A的产生。这些结果表明,在其吸附的构象中,潮湿能够通过TLRS诱导巨噬细胞的有效的促炎反应,并且应该进一步研究TLR信号传导途径,以调节对植入生物材料的宿主反应的潜在治疗靶标。

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