Scotece Morena, Pérez Tamara, Conde Javier, Abella Vanessa, López Veronica, Pino Jesús, Gonzalez-Gay Miguel A, Gomez-Reino Juan J, Mera Antonio, Gomez Rodolfo, Gualillo Oreste
SERGAS (Servizo Galego de Saude) and IDIS (Instituto de Investigación Sanitaria de Santiago), Research Laboratory 9 (NEIRID LAB: Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Santiago University Clinical Hospital, Building C, Level-2, Door 9, Santiago de Compostela 15706, Spain.
SERGAS-IDIS, Division of Orthopaedic Surgery and Traumatology, Santiago University Clinical Hospital, Santiago de Compostela, Spain.
J Orthop Res. 2017 Jun;35(6):1299-1303. doi: 10.1002/jor.23377. Epub 2017 Mar 28.
Osteoarthritis (OA) is a chronic systemic musculoskeletal disorder involving inflammation, immunity, and metabolic alterations. OA is commonly regarded as non-inflammatory disease; still inflammation is recognized as contributing to the symptoms and progression of OA. New evidence suggests that adipokines are involved in the pathophysiology of OA and might modulate the production of inflammatory mediators including in immune cells. However, the role of immune component in osteoarthritis is still poorly investigated. To gain further insights into the interaction of immune cells in OA and the role of adipokines on these cells, we performed experiments aimed to determine the cytokine profile in activated CD4 T cells from OA patients. For completeness, we also explored the cross talk between T lymphocytes and chondrocytes in OA by co-culturing human primary chondrocytes with activated CD4 T cells in two ways: the first by incubating the cells by direct contact (D.C.) or by transwell system. Our results show that the exposure of activated CD4 T cells to adipokines modulates IL-6, IL-8, and CCL-3 production. In addition, the production of key macromolecules of ECM (aggrecan and collagen-2) and matrix metalloproteinase 13 (MMP-13) in co-cultured chondrocytes with activated CD4 T cells was altered. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1299-1303, 2017.
骨关节炎(OA)是一种慢性全身性肌肉骨骼疾病,涉及炎症、免疫和代谢改变。OA通常被视为非炎症性疾病;然而,炎症仍被认为是导致OA症状和病情进展的因素。新证据表明,脂肪因子参与OA的病理生理过程,并可能调节包括免疫细胞在内的炎症介质的产生。然而,免疫成分在骨关节炎中的作用仍研究不足。为了进一步深入了解OA中免疫细胞的相互作用以及脂肪因子对这些细胞的作用,我们进行了实验,旨在确定OA患者活化CD4 T细胞中的细胞因子谱。为了全面起见,我们还通过两种方式将人原代软骨细胞与活化CD4 T细胞共培养,探讨了OA中T淋巴细胞与软骨细胞之间的相互作用:第一种是通过直接接触(D.C.)孵育细胞,第二种是通过Transwell系统。我们的结果表明,活化CD4 T细胞暴露于脂肪因子会调节IL-6、IL-8和CCL-3的产生。此外,与活化CD4 T细胞共培养的软骨细胞中细胞外基质(聚集蛋白聚糖和胶原-2)和基质金属蛋白酶13(MMP-13)的关键大分子产生发生了改变。©2017骨科研究协会。由Wiley Periodicals, Inc.出版。《矫形外科研究杂志》35:1299 - 1303, 2017。