血管活性肠肽调节骨关节炎和类风湿性关节炎滑膜细胞中促炎介质的合成。

Vasoactive intestinal peptide modulates proinflammatory mediator synthesis in osteoarthritic and rheumatoid synovial cells.

作者信息

Juarranz M G, Santiago B, Torroba M, Gutierrez-Cañas I, Palao G, Galindo M, Abad C, Martinez C, Leceta J, Pablos J L, Gomariz R P

机构信息

Departamento de Biología Celular, Facultad de Biología, Universidad Complutense de Madrid, Spain.

出版信息

Rheumatology (Oxford). 2004 Apr;43(4):416-22. doi: 10.1093/rheumatology/keh061. Epub 2003 Dec 1.

Abstract

OBJECTIVE

Vasoactive intestinal peptide (VIP) has demonstrated beneficial effects in several murine models of immune-mediated inflammation by inhibiting both the inflammatory and the autoimmune components of the disease. We investigate its potential to modulate the release of proinflammatory cytokines and chemokines by human synovial cells from patients with rheumatoid arthritis (RA).

METHODS

Fresh suspensions of synovial tissue cells (STC) or cultured fibroblast-like synoviocytes (FLS) were obtained from patients with RA or osteoarthritis (OA). The effects of VIP on basal or tumour necrosis factor alpha (TNF-alpha)-stimulated production of CCL2 (MCP-1, monocyte chemotactic protein 1), CXCL8 [interleukin (IL)-8], IL-6 and TNF-alpha were studied by specific ELISAs (enzyme-linked immunosorbent assays). The mRNAs for CCL2, CXCL8 and IL-6 in FLS were analysed by real-time reverse transcription-polymerase chain reaction.

RESULTS

VIP at 10 nm down-regulated chemokine production by STC and FLS from RA and OA patients. VIP also down-regulated the expression of mRNAs for CCL2, CXCL8 and IL-6. The effects of VIP were more clearly detected in RA samples and after stimulation with TNF-alpha.

CONCLUSION

Our observations confirm that the proposed anti-inflammatory actions of VIP in murine models also apply to human synovial cells ex vivo. Further studies are encouraged to evaluate the use of VIP as a potential therapy for chronic inflammatory joint diseases.

摘要

目的

血管活性肠肽(VIP)在几种免疫介导的炎症小鼠模型中已显示出有益作用,可抑制疾病的炎症和自身免疫成分。我们研究其调节类风湿关节炎(RA)患者人滑膜细胞促炎细胞因子和趋化因子释放的潜力。

方法

从RA或骨关节炎(OA)患者获取滑膜组织细胞(STC)的新鲜悬液或培养的成纤维细胞样滑膜细胞(FLS)。通过特异性酶联免疫吸附测定(ELISA)研究VIP对基础状态或肿瘤坏死因子α(TNF-α)刺激下CCL2(单核细胞趋化蛋白1,MCP-1)、CXCL8[白细胞介素(IL)-8]、IL-6和TNF-α产生的影响。通过实时逆转录-聚合酶链反应分析FLS中CCL2、CXCL8和IL-6的mRNA。

结果

10 nM的VIP下调了RA和OA患者STC和FLS趋化因子的产生。VIP还下调了CCL2、CXCL8和IL-6的mRNA表达。在RA样本中以及TNF-α刺激后,更明显地检测到了VIP的作用。

结论

我们的观察结果证实,VIP在小鼠模型中提出的抗炎作用也适用于体外培养的人滑膜细胞。鼓励进一步研究评估将VIP用作慢性炎症性关节疾病的潜在治疗方法。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索