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VIP Decreases TLR4 Expression Induced by LPS and TNF-a Treatment in Human Synovial Fibroblasts

机译:VIP降低了LPS和TNF-A治疗在人类滑膜成纤维细胞中的诱导的TLR4表达

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It has been demonstrated that VIP produces beneficial effects both in a murine model of rheumatoid arthritis and in human rheumatoid synovial fibroblasts through the modulation of proinflammatory mediators. Toll-like receptors (TLRs) play a key role in the immediate recognition of microbial surface components by immune cells prior to the development of adaptative microbe-specific immune responses. In this study, we demonstrate that VIP decreases lipopolysaccharide (LPS) and TNF-α -induced expression of TLR4 and its correlation with the production of CCL2 and CXCL8 chemokines in human synovial fibroblasts from patients with rheumatoid arthritis and osteoarthritis. Our results add a new step for the use of VIP, as a promising candidate, for the treatment of rheumatoid arthritis.
机译:已经证明,通过调节促炎介质,VIP在类风湿性关节炎的鼠模型和人类风湿性滑膜成纤维细胞中产生有益效果。在发育适应性微生物特异性免疫应答之前,可以在立即识别微生物表面组分的立即识别微生物表面组分中发挥关键作用。在该研究中,我们证明VIP降低了脂多糖(LPS)和TNF-α-诱导的TLR4表达及其与来自类风湿性关节炎和骨关节炎患者的人类滑膜成纤维细胞中的CCL2和CXCL8趋化因子的相关性。我们的结果为使用VIP作为一个有前途的候选者添加了一种新的步骤,用于治疗类风湿性关节炎。

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