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间皮细胞增殖:对与纤维化相关的肺损伤的非特异性反应。

Mesothelial cell proliferation: a nonspecific response to lung injury associated with fibrosis.

作者信息

Adamson I Y, Bakowska J, Bowden D H

机构信息

Department of Pathology, University of Manitoba, Winnipeg, Canada.

出版信息

Am J Respir Cell Mol Biol. 1994 Mar;10(3):253-8. doi: 10.1165/ajrcmb.10.3.7509611.

Abstract

An early proliferative response of mesothelial and subpleural cells has been reported in animals after inhalation or intratracheal (I.T.) instillation to the lung of long asbestos fibers, which also induce pulmonary fibrosis. To determine whether this cell proliferation is directly related to asbestos exposure or is a nonspecific response to injury, we examined [3H]thymidine (3HT) uptake by cells at the pleura after exposing mice to 5 days of hyperoxia, to intravenous (I.V.) (3 mg) or I.T. (0.15 mg) bleomycin, to I.T. (1 mg) silica, and to I.T. (0.1 mg) crocidolite asbestos of mixed length. All exposures induced acute lung injury, as shown by high levels of protein in lavage fluid. After hyperoxia, the percentage of total lung cells labeled by 3HT in autoradiographs was high for only a few days, as repair took place with no increase in fibroblast growth and no subsequent development of fibrosis. Particle or bleomycin exposure induced a prolonged increase in 3HT uptake with enhanced fibroblast labeling over a 4- to 6-wk period. In each case, labeled subpleural cells, mainly fibroblasts, increased up to 10-fold in the first 2 to 4 wk. At the same time, 3HT uptake by mesothelial cells ranged from 1.4 to 3% compared with almost zero in controls and in oxygen-exposed mice after a few days upon return to air. These results indicate that mesothelial and subpleural cell proliferation occurs after various types of injury to the lung. The close temporal association between 3HT uptake by mesothelial cells and fibroblasts during the reparative phase suggests that mesothelial cells may respond to the same cytokines that trigger interstitial fibrosis.

摘要

据报道,动物吸入或经气管内(I.T.)滴注长石棉纤维至肺部后,间皮细胞和胸膜下细胞会出现早期增殖反应,长石棉纤维也会诱发肺纤维化。为了确定这种细胞增殖是与石棉暴露直接相关,还是对损伤的非特异性反应我们在将小鼠暴露于5天的高氧环境、静脉内(I.V.)(3mg)或经气管内(0.15mg)博来霉素、经气管内(1mg)二氧化硅以及经气管内(0.1mg)混合长度的青石棉后,检测了胸膜处细胞对[3H]胸腺嘧啶核苷(3HT)的摄取情况。所有暴露均诱发了急性肺损伤,灌洗液中蛋白质水平升高即表明了这一点。高氧暴露后,放射自显影片中被3HT标记的肺细胞总数的百分比仅在几天内较高,因为修复过程中没有成纤维细胞生长增加,也没有随后的纤维化发展。颗粒或博来霉素暴露导致3HT摄取持续增加,在4至6周内成纤维细胞标记增强。在每种情况下,标记的胸膜下细胞,主要是成纤维细胞,在最初2至4周内增加了多达10倍。与此同时,间皮细胞对3HT的摄取范围为1.4%至3%,而对照组和高氧暴露小鼠在恢复空气环境几天后几乎为零。这些结果表明,肺受到各种类型损伤后会发生间皮细胞和胸膜下细胞增殖。修复阶段中间皮细胞和成纤维细胞对3HT摄取之间紧密的时间关联表明,间皮细胞可能对触发间质纤维化的相同细胞因子产生反应。

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