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首页> 外文期刊>Cell and Tissue Research >Anaphylatoxin receptors and complement regulatory proteins in human articular and non-articular chondrocytes: Interrelation with cytokines
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Anaphylatoxin receptors and complement regulatory proteins in human articular and non-articular chondrocytes: Interrelation with cytokines

机译：人关节和非关节软骨细胞中过敏毒素受体和补体调节蛋白：与细胞因子的相互关系

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摘要

Tissue trauma induces an inflammatory response associated with a cytokine release that may engage complement pathways. Cytokine-mediated complement expression may contribute to cartilage degradation. Hence, we analysed the complement expression profile in primary articular and non-articular chondrocytes and its interrelation with cytokines. The expression of the anaphylatoxin receptors (C3aR and C5aR) and the complement regulatory proteins (CPRs) CD35, CD46, CD55 and CD59 was studied in cultured articular, auricular and nasoseptal chondrocytes using RTD-PCR and immunofluorescence labelling. The complement profile of peripheral blood mononuclear cells (PBMCs) was opposed to the expression in articular chondrocytes. The time-dependent regulation (6 and 24 h) of these complement factors was assessed in articular chondrocytes in response to the cytokines TNFa, IL-10 or TNFa combined with IL-10 (each 10 ng/mL). C3aR, C5aR, CD46, CD55 and CD59 but almost no CD35 mRNA was expressed in any of chondrocyte types studied. The anaphylatoxin receptor expression was lower and that of the CRPs was higher in chondrocytes when compared with PBMCs. The majority of the studied complement factors were expressed at a significantly lower level in non-articular chondrocytes compared with the articular chondrocytes. TNFa significantly increased the C3aR expression in chondrocytes after 6 and 24 h. TNFa + IL-10 significantly downregulated C5aR and IL-10 significantly inhibited the CD46 and CD55 gene expression after 24 h. C5aR and CD55 could be localised in cartilage in situ. Anaphylatoxin receptors and CRPs are regulated differentially by TNFa and IL-10. Whether cytokine-induced complement activation occurs in response to cartilage trauma has to be further identified.
机译：组织创伤引起与细胞因子释放相关的炎症反应，可能参与补体途径。细胞因子介导的补体表达可能导致软骨降解。因此，我们分析了原发性关节和非关节软骨细胞的补体表达谱及其与细胞因子的相互关系。使用RTD-PCR和免疫荧光标记法研究了培养的关节，耳和鼻中隔软骨细胞中过敏毒素受体（C3aR和C5aR）和补体调节蛋白（CPR）CD35，CD46，CD55和CD59的表达。外周血单核细胞（PBMC）的补体谱与关节软骨细胞中的表达相反。响应细胞因子TNFa，IL-10或TNFa与IL-10（各10 ng / mL）的反应，评估了关节软骨细胞中这些补体因子的时间依赖性调节（6和24小时）。 C3aR，C5aR，CD46，CD55和CD59，但几乎没有CD35 mRNA在任何研究的软骨细胞类型中表达。与PBMC相比，软骨细胞中过敏毒素受体的表达较低，而CRP的表达较高。与关节软骨细胞相比，大多数研究的补体因子在非关节软骨细胞中的表达水平明显较低。 6和24小时后，TNFa显着增加软骨细胞中C3aR的表达。 24小时后，TNFa + IL-10显着下调C5aR，IL-10显着抑制CD46和CD55基因表达。 C5aR和CD55可以原位定位在软骨中。过敏毒素受体和CRP受TNFa和IL-10的差异调节。是否必须响应软骨损伤而发生细胞因子诱导的补体激活。

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