尼古丁对人树突状细胞的激活及其与急性冠状动脉综合征的关系

Effects of Nicotine on Activation of Dendritic Cells in Acute Coronary Syndrome

目的 :研究尼古丁对人树突状细胞 (DC)功能的影响及其与急性冠状动脉综合征 (ACS)发病的关系。方法 :观察体外尼古丁对DC功能的作用以及 11例正常对照者 (正常对照组 )与 45例ACS者 (ACS组 )发病时及戒烟后DC的功能状态。流式细胞仪检测DCCD86的表达 ;混合淋巴反应检测DC对T淋巴细胞的刺激作用 ;酶联免疫吸附法 (ELISA)测定混合淋巴反应上清液中细胞因子水平。结果 :与正常对照组比较 ,ACS时DC表面CD86的表达明显增高 ,对T淋巴细胞刺激的能力增强 ;致炎细胞因子分泌增多 ;DCCD86的表达与日吸烟量正相关 (r =0 63 ,P <0 0 1) ;平均戒烟 5个月后 ,DC功能接近正常 ;体外尼古丁亦能明显刺激DC的功能 ,呈浓度依赖性。结论 :①ACS时DC明显激活 ;②戒烟后DC功能可迅速恢复 ;③尼古丁可能是ACS时DC激活的刺激因素之一。

Objective:To investigate the effects of nicotine on function of dendritic cells(DC) and its relation to acute coronary syndrome(ACS). Methods:Periphery blood monocyte cells(PBMC) from 45 patients with,ACS(after onset of the disease and smoking cessation)and 11 healthy subjects were incubated and induced to mature DC in a completed medium containing GM-CSF and IL-4.The flow cytometric analysis were used to detect the expression of co-stimulating factor CD86(B7-2)on DC.The stimulating capacity of DC was determined in allogenic mixed lymphocyte reaction(MLR).ELISA was used to analyze the level of cytokines(IL-1β,IL-6,and TNF-a) in the medium of MLR and in the blood. Relationship of expression of CD86 to cardiovascular risk factors was also analyzed. In vitro stimulating effects of nicotine on DC were also investigated.Results:When compared with the normal group,CD86 on DC was much more expressed in ACS;the stimulating capacity of DC in MLR was higher;and the T lymphocytes in MLR produced higher levels of pro-inflammation cytokines(IL-1β,IL-6,and TNF-a). CD86 was positively correlated with the amount consumed per day.After quitting smoking for 5 months,their DC function recovered to normal. In vitro,nicotine stimulated DC significantly,which was dose-dependent.Conclusion:①DCs in ACS are activated,which may play an important role in initiating immune reaction in the events. ②The activation of DC in ACS may be mediated by nicotine.③Quitting smoking results in recovery of DC function.