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牛Ⅱ型胶原蛋白诱导VSIG4-/-鼠的关节炎模型

Induction of rheumatoid arthritis in VSIG4-/- mice by bovine type Ⅱ collagen

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【作者】 金美花费蕾陈永文李春实

【Author】 JIN Meihua;FEI Lei;CHEN Yongwen;LI Chunshi;Department of Pharmacology,Yanbian University College of Medicine;Institute of Immunology,PLA,Third Military Medical University;

【机构】 延边大学医学院药理学教研室第三军医大学全军免疫学研究所

【摘要】 目的以Ⅱ型胶原蛋白诱导的VSIG4-/-(C57BL-6背景)小鼠关节炎模型为研究对象,探讨VSIG4在RA疾病进程中的作用。方法取SPF级DBA/1、VSIG4-/-(C57BL-6背景)以及Ncf1-/-(C57BL-6背景)小鼠,以牛Ⅱ型胶原蛋白(CⅡ)与完全佛氏佐剂完全乳化,尾根部皮下注射,在第21天以牛Ⅱ型胶原蛋白与不完全弗氏佐剂加强免疫获得CIA模型。定期观察小鼠关节改变,并进行关节评分。用H&E染色法观察小鼠关节组织病理学改变并采用流式细胞术检测脾淋巴细胞以及腹腔巨噬细胞中TNF-α的变化。结果与Ncf1-/-及DBA/1小鼠相似,VSIG4-/-小鼠在牛Ⅱ型胶原蛋白免疫后开始出现明显的多关节肿胀,即小鼠踝关节病理检测显示明显的滑膜增生,炎症细胞浸润以及关节坏死。进一步研究发现来源于VSIG4-/-关节炎模型小鼠与同系正常小鼠相比,虽然脾淋CD4+T巴细胞分泌的TNF-α没有显著性差异(P>0.05),但是腹腔巨噬细胞分泌的TNF-α具有显著性差异(P<0.05)。结论牛Ⅱ型胶原蛋白可诱导VSIG4-/-小鼠的关节炎,而腹腔巨噬细胞分泌的TNF-α在其发病过程中可能起关键作用。

【Abstract】 This study designed to observe the effect of VSIG4 in the progress of rheumatoid arthritis by using the collagen-induced arthritis model of VSIG4-/-(genetic background: C57BL/6) mice. The CIA mouse model was established by immunization of VSIG4-/-(genetic background: C57BL/6) mice, DBA/1 mice and Ncf1-/-(genetic background: C57BL/6) mice with emulsified bovine type Ⅱ(C Ⅱ) in complete Freund via subcutaneous injection.Additionally, mice were also given booster injection of C Ⅱ in incomplete Freund at day 21 after the first immunization. The joint ailment was detected by H&E staining, and the frequencies of TNF-α from splenic lymphocyte and peritoneal macrophage were detected by flow cytometry. The signaling of arthritis development of VSIG4-/-and Ncf1-/-mice were visible at day 9 after first immunization. Although there were no significant differences of TNF-α+CD4+T cells between VSIG4-/-CIA mice and VSIG4-/-littermates, the levels of TNF-α+F4/80+peritoneal macrophages were significantly higher in VSIG4-/-CIA mice(P < 0.05). These combined data suggest that VSIG4 involves in the pathogenesis of RA, and the higher levels of TNF-α from VSIG4-/-peritoneal macrophages should involve in the pathogenesis.

【基金】 国家自然科学基金(61361013)
  • 【文献出处】 免疫学杂志 ,Immunological Journal , 编辑部邮箱 ,2015年03期
  • 【分类号】R593.22;R-332
  • 【被引频次】3
  • 【下载频次】225
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