Tolusso Barbara, Alivernini Stefano, Gigante Maria Rita, Ferraccioli Gianfranco, Gremese Elisa
a Division of Rheumatology, Institute of Rheumatology , Catholic University of the Sacred Heart , Rome , Italy.
Expert Rev Clin Immunol. 2016 Jul;12(7):751-62. doi: 10.1586/1744666X.2016.1159132. Epub 2016 Mar 22.
Adipose tissue is an active organ playing a role not only in metabolism but also in immune and inflammatory processes, releasing several pro-inflammatory mediators. This can explain the possible association between obesity and rheumatoid arthritis (RA) and its role in the progression of the disease. Adipose and synovial tissues share common histological features of local inflammation in terms of activation of target tissues infiltrating cells (i.e. myeloid cells). Among the so-called adipocytokines, PEDF and Chemerin orchestrate the cellular cross-talk between adipose and myeloid cells, being possible biomarkers to monitor the effect of weight loss or the decrease of adipose tissue in patients with RA. Moreover, dietary intervention has been demonstrated to reduce Chemerin as well as IL-6 and MCP-1 expression. Finally, epigenetic regulators such as micro-RNAs (i.e. miR-155) are key regulators of myeloid cells activation in RA and obesity as well as in adipocytes. In this review, we will summarize the biological link between obesity/overweight state and RA focusing on pathophysiological mechanisms, consequences and management considerations.
脂肪组织是一个活跃的器官,不仅在新陈代谢中发挥作用,还在免疫和炎症过程中发挥作用,释放多种促炎介质。这可以解释肥胖与类风湿性关节炎(RA)之间可能存在的关联及其在疾病进展中的作用。脂肪组织和滑膜组织在靶组织浸润细胞(即髓样细胞)激活方面具有局部炎症的共同组织学特征。在所谓的脂肪细胞因子中,色素上皮衍生因子(PEDF)和瑞托菌素(Chemerin)协调脂肪细胞与髓样细胞之间的细胞相互作用,可能是监测RA患者体重减轻或脂肪组织减少效果的生物标志物。此外,饮食干预已被证明可降低Chemerin以及白细胞介素-6(IL-6)和单核细胞趋化蛋白-1(MCP-1)的表达。最后,表观遗传调节因子如微小RNA(即miR-155)是RA、肥胖以及脂肪细胞中髓样细胞激活的关键调节因子。在本综述中,我们将总结肥胖/超重状态与RA之间的生物学联系,重点关注病理生理机制、后果及管理考量因素。