结核分枝杆菌及抗原ESAT-6、Ag85B对中性粒细胞白三烯B4表达的影响  被引量:1

Effects of Mycobacterium Tuberculosis and Antigen85B,ESAT-6 on Leutriene B4 Production from Human Neutrophil

在线阅读下载全文

作  者:赵青[1] 冯国栋[1] 王雯菁 朱旗[1] 张敏[1] 刘扬[1] 史明[1] 赵钢[1] 

机构地区:[1]第四军医大学西京医院神经内科,西安710032

出  处:《医学研究杂志》2015年第5期20-24,共5页Journal of Medical Research

基  金:国家自然科学基金资助项目(81371334)

摘  要:目的观察结核分枝杆菌及其抗原成分对人外周血中性粒细胞白三烯B4表达的影响。方法 ELISA法检测结核分枝杆菌不同菌株及抗原分别与外周血中性粒细胞共培养上清白三烯B4及相关细胞因子TNF-α表达量,应用花生四烯酸代谢通路抑制剂来探讨其可能的机制。结果 BCG、ESAT-6、Ag85B刺激中性粒细胞生成白三烯B4和TNF-α、ESAT-6、Ag85B刺激生成LTB4呈剂量依赖,H37Ra不引起LTB4表达但可增加TNF-α表达,Ag85B刺激生成的LTB4可被齐留通和苯丁抑制素阻断,但对TNF-α表达无明显影响。结论卡介苗及ESAT-6、Ag85B诱导人中性粒细胞产生LTB4和TNF-α,Ag85B诱导的LTB4可被抑制剂阻断但不影响TNF-α表达。感染早期中性粒细胞通过生成LTB4发挥抗结核作用。Objective To study the effects of Mtb and antigen on leutrinene B4 production from human neutrophil. Methods The fresh peripheral blood samples from healthy adults were incubated with Mtb and antigen at different dose. Supernatants were collected for LTB4 and TNF -α detection by ELISA. Pharmacological inhibitors of leukotrienes synthesis was used to find possible mechanism. Results In this study we found that neutrophils could release LTB4 and TNF -α induced by BCG,ESAT -6 and Ag85B. ESAT-6 - and Ag85B - activated human PMN secreting the LTB4 in a dose dependent manner. Neutrophils did not produce LTB4 in response to H37Ra. Treat- ment of PMN with the leukotriene B4 inhibitor Zileuton or Bestatin prior to stimulation with Ag85B partially blocked LTB4 induction but did not work on TNF - a production. Conclusion BCG,ESAT - 6, Ag85B may induce neutrophil activation and enhance LTB4 release. These effects can be reduced by arachidonic acid metabolism pathway inhibitors of Zileuton and Bestatin which did not work on TNF - α production. We conclude that PMN contribute to early resistance to Mtb via LTB4 secretion.

关 键 词:结核分枝杆菌 AG85B ESAT-6 白三烯B4 中性粒细胞 

分 类 号:R3[医药卫生—基础医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象