脂多糖致肺血管内巨噬细胞释放炎症因子变化的研究  

Changes in inflammatory cytokines released by pulmonary intravascular macrophages after stimulation with lipopolysaccharide

作　　者：李胜亮 张淑琴 秦翠平 陈彬 陈正堂[2] 金敬顺[2] 伍伟玲[2] 

机构地区：[1]解放军第五一七医院内科,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：《中国危重病急救医学》2006年第3期136-138,共3页Chinese Critical Care Medicine

基　　金：国家自然科学基金资助项目(39800064)

摘　　要：目的探讨肺血管内巨噬细胞(P IM)在感染性急性肺损伤(AL I)发病中的作用。方法按照M orton法分离、培养猪P IM,予10 m g/L脂多糖(LPS)刺激,酶联免疫吸附法(EL ISA)测定肿瘤坏死因子α(TNFα)、白细胞介素6(IL 6)和IL 8的含量。结果LPS刺激后,P IM释放TNFα、IL 6和IL 8增多,峰值分别出现在刺激后的1、4和6 h,与刺激前相比,差异均有显著性(P均<0.01)。结论LPS刺激后,P IM分泌多种细胞因子,其中TNFα升高最早,提示其在AL I发病早期起重要作用;而IL 6、IL 8升高较晚,且后者持续时间较长,可能对AL I的病情进展起重要作用。细胞因子间的相互作用在AL I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 lipopolysaceharide （LPS, 10 mg/L ）. The contents of interleukin- 6 （IL- 6）, IL-8 and tumor necrosis factor-α（TNF -α） in the culture supernatants were respectively measured by enzyme linked immunoadsorbent assay （ELISA）. Results The release of TNF -α, IL- 6 and IL -8 by PIMs was increased significantly as compared with the levels before stimulation by LPS, peaking at I, 4, and 6 hours after LPS stimulation, respectively. The differences were significant （all P〈0. 01）. Conclusion Among the cytokines released by PIMs after LPS challenge, the increase in TNF -α content occurs earlier in comparison with that of IL - 6 and 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 - 6 and IL - 8 contents is later than that of TNF -α and lasts for a longer time, suggesting that they may be associated with the development of ALI. The results also suggest 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  肺损伤.急性 

分 类 号：R363[医药卫生—病理学]