The role of properdin in murine zymosan-induced arthritis
The role of properdin in murine zymosan-induced arthritis
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DOI：
10.1016/j.molimm.2010.02.007
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发表时间：
2010-04-01
影响因子：
3.6
通讯作者：
Stover, Cordula
中科院分区：
文献类型：
--
作者：
Dimitrova, Petya;Ivanovska, Nina;Stover, Cordula
利用缺乏备解素和野生型的小鼠，我们研究了备解素在酵母多糖诱导的关节炎发生和发展中的作用。在酵母多糖诱导局部炎症的初期，备解素缺陷型和野生型小鼠表现为骨质侵蚀、蛋白多糖丢失和细胞浸润。与野生型相比，缺乏备解素的小鼠的C5a和IL-6水平降低，但滑膜中的INF-α和sRANKL水平相似。这两组人都表现出了全身免疫反应。在备解素缺乏的小鼠中，观察到脾细胞中干扰素-γ的产生和STAT1信号的增加，以及延髓淋巴结中Th1反应的转变。与野生型相比，缺乏备解素的小鼠循环中酵母多糖特异性的抗体显著减少。在慢性期，缺乏备解素导致关节蛋白多糖显著丢失，软骨细胞STAT1表达降低。在第30天，两组滑液中C5a的水平是相似的，但C5aR染色在缺乏备解素的小鼠的关节中更明显。我们的数据显示，备解素在炎性关节降解过程中发挥着重要作用。(C)2010爱思唯尔有限公司。保留所有权利。
Using properdin-deficient and wild-type mice, we have investigated the role of properdin in development and progression of zymosan-induced arthritis. At the initial phase of local, zymosan-induced inflammation, properdin-deficient and wild-type mice showed bone erosion, proteoglycan loss and cell infiltration. Compared to wild-type, properdin-deficient mice had reduced C5a and IL-6 but similar synovial INF-alpha and sRANKL levels. Both groups showed a systemic immune response. Elevated IFN-gamma production and STAT1 signaling in splenocytes and a shift to Th1 response in popliteal lymph nodes were observed in properdin-deficient mice. Properdin-deficient mice had significantly less circulating zymosan-specific IgG antibodies than wild-type. In the chronic phase, the lack of properdin resulted in significant proteoglycan loss in the joints and lower cartilageneous STAT1 expression. The level of synovial C5a on day 30 was comparable in both groups, but C5aR staining was more apparent in the joints of properdin-deficient mice. Our data show that properdin is an important player in processes involved in inflammatory joint degradation. (C) 2010 Elsevier Ltd. All rights reserved.