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首页> 外文期刊>Thorax: The Journal of the British Thoracic Society >The alveolar epithelium can initiate the extrinsic coagulation cascade through expression of tissue factor.
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The alveolar epithelium can initiate the extrinsic coagulation cascade through expression of tissue factor.

机译：肺泡上皮可以通过组织因子的表达引发外在凝血级联反应。

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BACKGROUND: The alveolar compartment is a procoagulant antifibrinolytic environment in acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS). A study was undertaken to test the hypothesis that the alveolar epithelium can initiate intra-alveolar coagulation by expressing active tissue factor (TF). METHODS: Using an in vitro cell surface TF assay and TF ELISA, the activity and production of TF in cultured alveolar epithelial (A549) cells following exposure to cytomix (tumour necrosis factor alpha, interleukin 1beta and interferon gamma) was measured. TF gene transcription was measured by semi-quantitative reverse-transcription PCR. Immunohistochemistry for TF was performed on lung sections from patients with ARDS and controls. TF protein levels were measured by ELISA in undiluted pulmonary oedema fluid from patients with ALI/ARDS and compared with control patients with hydrostatic pulmonary oedema. RESULTS: TF activity, mRNA and protein levels increased in A549 cells after stimulation with cytomix. Increased TF activity was also seen in A549 cells following incubation with pulmonary oedema fluid from patients with ALI/ARDS. Immunohistochemistry for TF in human lung tissue from patients with ARDS showed prominent TF staining in alveolar epithelial cells as well as intra-alveolar macrophages and hyaline membranes. TF antigen levels in oedema fluid (median 37 113 (IQR 14 956-73 525) pg/ml) were significantly higher than in plasma (median 336 (IQR 165-669) pg/ml, p<0.001) in patients with ALI/ARDS, and TF procoagulant activity in oedema fluid was much higher than in plasma of these patients. Higher plasma levels were associated with mortality. CONCLUSIONS: The alveolar epithelium is capable of modulating intra-alveolar coagulation through upregulation of TF following exposure to inflammatory stimuli and may contribute to intra-alveolar fibrin deposition in ARDS.
机译：背景：肺泡腔是急性肺损伤（ALI）和急性呼吸窘迫综合征（ARDS）的促凝抗纤溶环境。进行了一项研究以检验以下假设：肺泡上皮可以通过表达活性组织因子（TF）来引发肺泡内凝血。方法：使用体外细胞表面TF测定和TF ELISA，测量暴露于细胞混合物（肿瘤坏死因子α，白介素1β和干扰素γ）后培养的肺泡上皮（A549）细胞中TF的活性和产生。 TF基因转录通过半定量逆转录PCR测量。 TF的免疫组织化学是在ARDS和对照患者的肺切片上进行的。通过ELISA测定ALI / ARDS患者未稀释的肺水肿液中的TF蛋白水平，并与对照组的静水性肺水肿进行比较。结果：细胞混合液刺激后，A549细胞的TF活性，mRNA和蛋白质水平增加。与ALI / ARDS患者的肺水肿液一起孵育后，A549细胞中的TF活性也增加。 ARDS患者人肺组织中TF的免疫组织化学分析显示，肺泡上皮细胞以及肺泡内巨噬细胞和透明膜上有明显的TF染色。 ALI /这些患者的水肿液中的ARDS和TF促凝活性远高于血浆中。较高的血浆水平与死亡率有关。结论：肺泡上皮能够通过暴露于炎性刺激后通过上调TF来调节肺泡内凝血，并可能促进ARDS中肺泡内纤维蛋白的沉积。

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