脂多糖致肺血管内巨噬细胞释放TNFα-、IL-1β及IL-8的改变  

Changes of TNF-αIL-1β and IL-8 released by pulmonary intravascular macrophages(PIMs)after stimulation with Lipopolysaccharide

作　　者：李胜亮 张淑琴 武志宏 秦翠萍 栗涛 陈正堂[2] 金敬顺[2] 马素凤 李佳 

机构地区：[1]解放军第517医院呼吸内科,山西岢岚036301 [2]第三军医大学新桥医院全军呼吸内科研究所,重庆400037

出　　处：《临床肺科杂志》2011年第1期4-5,共2页Journal of Clinical Pulmonary Medicine

基　　金：国家自然科学基金资助(编号:No39800064)

摘　　要：目的探讨肺血管内巨噬细胞(PIM)在感染性急性肺损伤(ALI)发病中的作用。方法仿Morton法灌洗肺血管床,贴壁法分离猪PIM,培养于RPM I 1640培养基,予10 mg/L脂多糖(LPS)刺激,胸腺细胞增殖法测PIM培养上清白细胞介素-1β(IL-1β)活性,酶联免疫吸附试验(ELISA)法测肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)含量。结果 LPS刺激后,PIM释放TNF-α、IL-1β和IL-8增多,峰值分别出现在刺激后的1、2和6 h。与刺激前相比,P<0.01。结论 LPS刺激后,PIM分泌多种细胞因子,其中TNFα-、IL-1β升高最早,提示其在ALI发病早期起重要作用;而IL-8升高较晚,且后者持续时间较长,可能对ALI的病情进展起重要作用。细胞因子间的相互作用在ALI的发病中似乎更为重要。Objective To investigate the roles of pulmonary Intravascular macrophages（PIMs）in the pathogenesis of infective acute lung injury（ALI）.Methods Porcine pulmonary blood vessels were flushed by modified Morton′s method,PIMs were isolated with adhesion method and incubated in RPMI 1640 medium.They were stimulated with lipopolysaccharide（LPS,10 mg/L）.The activity of interleukin-1β（IL-1β）and content of tumor necrosis factor-ɑ（TNF-ɑ）,interleukin-8（IL-8）in the culture supernatants were measured by method of thymocyte proliferation or enzyme linked immunoadsorbent assay（ELISA）,respectively.Results The releases of TNF-ɑ,IL-1β and IL-8 by PIMs was increased significantly as compared with level before stimulation by LPS,peaking at 1,2,and 6 hours after LPS stimulation,respectively.The difference were significant（P〈0.01）.Conclusions Among the cytokines released by PIMs after LPS challenge,the increase in TNF-ɑ and IL-1β occurs earlier in comparison with that of IL-8,suggesting that the former may play an important role at the early stage of ALI;on the other hand,the increase in IL-8 is later than that of TNF-ɑ,IL-1β and lasts for a longer time,suggesting that it may be associated with the development of ALI.The results also suggested that interaction of these cytokines is more important in the pathogenesis of ALI.

关 键 词：肺血管内巨噬细胞 细胞因子 急性肺损伤 脂多糖 

分 类 号：R563[医药卫生—呼吸系统]