Early tumor necrosis factor-α release from the pulmonary macrophage in lung ischemia-reperfusion injury
Early tumor necrosis factor-α release from the pulmonary macrophage in lung ischemia-reperfusion injury
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DOI：
10.1016/j.jtcvs.2003.08.019
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发表时间：
2004-05-01
影响因子：
6
通讯作者：
Mulligan, MS
中科院分区：
文献类型：
--
作者：
Naidu, BV;Woolley, SM;Mulligan, MS
目的：肿瘤坏死因子-a是一种促炎介质，在实验性肺缺血再灌注损伤的发生发展过程中起重要作用。在多种急性肺损伤模型中，肺泡巨噬细胞是肿瘤坏死因子-a的丰富来源。本研究旨在探讨肺泡巨噬细胞在肺缺血再灌注损伤中是否为肿瘤坏死因子-a的重要来源以及抑制其功能是否具有保护作用。方法：Long-Evans大鼠左肺常温缺血90min，再灌注4h。接受治疗的动物接受了氯化Gd，一种抑制巨噬细胞功能的稀土金属。通过肺组织中性粒细胞聚集(髓过氧化物酶含量)、肺血管通透性、支气管肺泡灌洗液中白细胞、细胞因子和趋化因子含量来量化损伤。结果：肿瘤坏死因子-α在再灌流15min时开始分泌，免疫组织化学显示肿瘤坏死因子-a定位于肺泡巨噬细胞。Gd组大鼠肺血管通透性在15min时下降66%(P
Objective: Tumor necrosis factor-a is a proinflammatory mediator required for the development of experimental lung ischemia-reperfusion injury. The alveolar macrophage is a rich source of tumor necrosis factor-a in multiple models of acute lung injury. The present study was undertaken to determine whether the alveolar macrophage is an important source of tumor necrosis factor-a in lung ischemiareperfusion injury and whether suppression of its function protects against injury.Methods: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours. Treated animals received gadolinium chloride, a rare earth metal that inhibits macrophage function. Injury was quantitated via lung tissue neutrophil accumulation (myeloperoxidase content), lung vascular permeability, and bronchoalveolar lavage fluid leukocyte, cytokine, and chemokine content. Separate samples were generated for immunohistochemistry.Results: Tumor necrosis factor-a secretion occurred at 15 minutes of reperfusion and was localized to the alveolar macrophage by immunohistochemistry. In gadolinium-treated animals, lung vascular permeability was reduced by 66% at 15 minutes (P