人主动脉瓣膜钙化过程中Th17/Treg细胞比率的变化

Change of Th17/Treg cells ratio in the process of aortic valve calcification

目的研究Th17/Treg细胞是否参与主动脉瓣膜钙化及其与瓣膜钙化发生相关的可能机制。方法人主动脉瓣膜组织分为3组(n=10):(1)对照组:瓣膜来自扩张型心肌病需心脏移植的受体,排除瓣膜组织病理改变者;(2)纤维化组:瓣膜来自严重主动脉瓣膜钙化需瓣膜置换术者,取远离瓣膜钙化部位,纤维化增生组织,排除风湿热及心内膜炎病史者;(3)钙化组:瓣膜来源同纤维化组,取瓣膜明显钙化组织。分别进行von kossa染色、免疫组织化学分析,用于进一步指导瓣膜组织分组;RT-PCR分析,检测瓣膜组织内Th17/Treg细胞浸润情况。结果对照组无Th17/Treg细胞浸润;纤维化组Th17细胞浸润明显高于钙化组(0.904±0.079比0.445±0.057,P<0.01);钙化组Treg细胞浸润明显高于纤维化组(0.900±0.058比0.396±0.032,P<0.01)。结论主动脉瓣膜钙化与纤维化组织中Th17/Treg细胞比率不同,调控Th17/Treg细胞分化趋势或许可以干预主动脉瓣膜钙化进程。

Objective To study whether Th17/Treg cell taking part in the development of aortic valve（ AV） calcification. Methods The tissue of AV was divided into three groups（ n = 10） ： control group,fibrous degeneration group and calcification group. Valve tissue in control group was taken from patients being subject to heart transplantation because of dilated cardiomyopathy,excluding valves with pathological change. Valve tissue in fibrous degeneration group was taken from location being away from calcification change,only fibrous thickening in patients being subject to valve replacement because of severe AV calcification,and excluding patients with rheumatism and endocarditis. Valve source in calcification group was the same of fibrous degeneration group,but taken from location being obvious calcification. Every sample was tested by von kossa stain or immunohistochemistry analysis and reverse transcription polymerase chain reaction（ RT-PCR）. Results Th17 /Treg cells were not present in control group. In fibrous degeneration group,the level of Th17 cell infiltration was significantly higher than that of calcification group（ 0.904 ±0.079 vs. 0.445 ±0.057,P〈0.01）. The level of Treg cell infiltration in calcification group was significantly higher than in fibrous degeneration group（ 0. 900 ± 0. 058 vs. 0. 396 ± 0. 032,P〈0. 01）.Conclusions The ratio of Th17 /Treg cells is different in aortic valve calcification and fibrosis tissue. By controlling the tendency of Th17 /Treg cells differentiation may interfere the progression of AV calcification.