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肿瘤坏死因子及其受体在鼠失血性休克引起的急性肺损伤中的作用
作者姓名:Song Y  Shi Y  Harken AH  Meng X  Raeburn CD
作者单位:1. 210002,南京,南京军区南京总医院呼吸内科
2. University of Colorado Health Sciences Center, School of Medicine, Denver CO 80262,USA
摘    要:目的 探讨失血性休克引起的急性肺损伤与肿瘤坏死因子-α(TNF—α)在肺组织表达的相关性。方法通过心腔穿刺对C57小鼠采取30%全血容量复制失血性休克模型。肺组织TNF-α表达采用酶联免疫吸附法方法进行测定。肺组织中性粒细胞(PMN)浸润采用数字荧光显微镜免疫荧光技术进行检测。肺微血管通透性(肺水肿)采用伊文氏蓝方法进行测定。结果(1)虽然失血性休克仅引起肺组织,TNF—α水平轻度和短暂的升高,且肺组织中性粒细胞(PMN)浸润时相上早于TNF-α水平的升高。但在,TNF基因剔除(K0)小鼠,失血性休克引起的肺组织PMN浸润和肺损伤明显轻于C57野生型小鼠;(2)给予失血前,TNF KO小鼠低水平的重组TNF-α即可导致失血性休克引起肺组织PMN浸润和急性肺损伤;(3)失血性休克引起的肺组织PMN浸润和急性肺损伤在p55TNF受体KO动物显著减轻,而在p75TNF KO动物则不产生影响。结论肺组织低水平TNF—α足以介导失血性休克引起的PMN浸润和急性肺损伤;p55TNF受体在失血性休克引起的肺部急性炎症反应中起主导作用。

关 键 词:肿瘤坏死因子  受体  失血性休克  急性肺损伤  多形核白细胞
修稿时间:2002年8月27日

A low level of TNF-mediates hemorrhage-induced acute lung injury via p55 TNF receptor
Song Y,Shi Y,Harken AH,Meng X,Raeburn CD.A low level of TNF-mediates hemorrhage-induced acute lung injury via p55 TNF receptor[J].National Medical Journal of China,2003,83(8):691-694.
Authors:Song Yong  Shi Yi  Harken Alden H  Meng Xianzhong  Raeburn Christopher D
Institution:Department of Respiratory Medicine, Nanjing General Hospital of PLA, Nanjing 210002, China.
Abstract:OBJECTIVE: To examine the temporal relationship of pulmonary TNF-alpha production to acute lung injury (ALI) during hemorrhagic shock (HS). METHODS: HS was induced in mice by removal of 30% of calculated total blood volume. Lung TNF-alpha was measured by ELISA. Lung neutrophil accumulation was detected by immunofluorescent staining, and pulmonary microvascular permeability was assessed using Evans blue dye. RESULTS: While HS induced a slight and transient increase in lung TNF-alpha, neutrophil accumulation preceded the change in lung TNF-alpha. However, lung neutrophil accumulation and the increase in microvascular permeability were abrogated in TNF-alpha knockout mice, and both were restored by administration of low dose TNF-alpha to TNF-alpha knockout mice prior to HS. Both neutrophil accumulation and microvascular leak were abrogated in p55 TNF-alpha receptor knockout mice, while p75 TNF-alpha receptor knockout mice behaved similar to wild type. CONCLUSION: A low level of pulmonary TNF-alpha is sufficient to mediate HS-induced acute lung injury and that the p55 TNF-alpha receptor plays a dominant role in regulating the pulmonary inflammatory response to HS. The results suggest that anti-TNF-alpha strategies for the control of the pulmonary inflammatory response to HS can be directed toward antagonizing the p55 TNF-alpha receptor.
Keywords:Gene knockout  Neutrophils  Microvascular permeability  Mouse
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