Juarranz Y, Gutiérrez-Cañas I, Arranz A, Martínez C, Abad C, Leceta J, Pablos J L, Gomariz R P
Departamento de Biología Celular, Facultad de Biología, UCM, 28040 Madrid, Spain.
Ann N Y Acad Sci. 2006 Jul;1070:359-64. doi: 10.1196/annals.1317.045.
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-alpha-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.
已经证明，血管活性肠肽（VIP）通过调节促炎介质，在类风湿性关节炎的小鼠模型和人类类风湿性滑膜成纤维细胞中均产生有益作用。Toll样受体（TLR）在适应性微生物特异性免疫反应发生之前，免疫细胞对微生物表面成分的即时识别中起关键作用。在本研究中，我们证明VIP可降低脂多糖（LPS）和肿瘤坏死因子-α（TNF-α）诱导的类风湿性关节炎和骨关节炎患者的人滑膜成纤维细胞中TLR4的表达及其与CCL2和CXCL8趋化因子产生的相关性。我们的结果为将VIP作为治疗类风湿性关节炎的有前景的候选药物的应用增加了新的步骤。
