rSj16, a recombinant protein of Schistosoma japonicum‐derived molecule, reduces severity of the complete Freund’s adjuvant‐induced adjuvant arthritis in rats’ model
rSj16, a recombinant protein of Schistosoma japonicum‐derived molecule, reduces severity of the complete Freund’s adjuvant‐induced adjuvant arthritis in rats’ model
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DOI：
10.1111/j.1365-3024.2010.01240.x
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发表时间：
2010-11
影响因子：
2.2
通讯作者：
X. Sun;Yongcheng Liu;Z. Lv;L. L. Yang-L.;S. Hu;H. Zheng;W. Hu;J. Cao;M. Fung;Z. Wu
中科院分区：
文献类型：
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作者：
X. Sun;Yongcheng Liu;Z. Lv;L. L. Yang-L.;S. Hu;H. Zheng;W. Hu;J. Cao;M. Fung;Z. Wu
Sj 16是日本血吸虫产生的一种16 kDa蛋白，已被证明具有抗炎作用。然而，这些现象的可能机制尚未被发现。本研究尝试用完全弗氏佐剂（CFA）诱导的大鼠关节炎模型进行接触。在CFA处理的大鼠中观察到一系列致病特征，包括局部和系统读出，这表明模型成功建立。rSj 16（重组Sj 16）体内给药后，足肿胀明显减轻，且呈剂量依赖性，血清中TNF-α、IL-1β和NO水平降低，IL-10水平升高。在体外，rSj 16逆转了脂多糖（LPS）诱导的骨髓来源的DC（BMDCs）中CD 80，CD 86，CD 54和OX 6的表面表达增加，而rSj 16处理的树突状细胞（DC）的内吞能力显著增加。从rSj 16处理的BMDC释放的IL-12 p70减少，但IL-10增加。此外，在与rSj 16致敏的BMDC孵育后，致敏的T细胞表现出抗炎性IL-10和IL-4的产生增加以及IL-12 p70和IFN-γ的产生减少。这些结果提示rSj 16可减轻CFA诱导的关节炎，其机制可能与阻断DC的成熟和功能有关。rSj 16可能是一种潜在的类风湿关节炎治疗药物。
Sj16, a 16‐kDa protein produced by Schistosoma japonicum, has been demonstrated to have anti‐inflammatory effect. However, the possible mechanism of these phenomena has not been discovered. Here, we tried to touch it with arthritis rats’ model induced by injection of complete Freund’s adjuvant (CFA). A set of pathogenic characters were observed in CFA‐treated rat, including local and systematic read‐out, which showed the model successfully set up. After administration of rSj16 (recombinant Sj16) in vivo, paw swelling reduced significantly and in a dose‐dependent manner, the level of TNF‐α, IL‐1β and NO decreased and IL‐10 in the serum increased. In vitro, rSj16 reversed the augmented surface expression of CD80, CD86, CD54 and OX6 induced by lipopolysaccharide (LPS) in bone marrow–derived DCs (BMDCs), whereas endocytotic capacity of rSj16‐treated dendritic cell (DC) was profoundly increased. IL‐12p70 released from rSj16‐treated BMDC was decreased but IL‐10 increased. Further, following incubation with rSj16 primed BMDCs, the sensitized T cells exhibited increased production of anti‐inflammatory IL‐10 and IL‐4 and decreased production of IL‐12p70 and IFN‐γ. Collectively, these results implied that rSj16 alleviated CFA‐induced arthritis, and the possible mechanisms may be its interruption of maturation and function of DCs. rSj16 could be a potential therapeutic agent against rheumatoid arthritis.