Pulmonary alveolar epithelium protects the lung through apoptosis of T lymphocytes

1. Fas/Fas配体在急性呼吸窘迫综合征（ARDS）中的表达及对T淋巴细胞凋亡的诱导作用我们检测了27例ARDS尸检肺中Fas/Fas配体（Fas L）的表达，并确定其是否诱导Fas阳性Jurkat T淋巴细胞凋亡。Fas在ARDS肺各期均有表达，Fas L在ARDS肺急性期肺泡上皮表达，在ARDS肺透明膜期和肺增生期表达减少。ARDS肺切片诱导Jurkat T淋巴细胞凋亡，在ARDS急性期发生率最高，在ARDS透明膜期和增殖期发生率降低。NOK-1预处理几乎完全抑制Jurkat T淋巴细胞的凋亡。提示肺泡上皮Fas - L的表达可能通过诱导淋巴细胞等促炎细胞凋亡起到保护肺损伤的作用。Fas/Pas配体在大鼠肺泡ⅱ型细胞中的表达及诱导T淋巴细胞凋亡的研究我们在大鼠离体肺泡II型细胞（II型细胞）中检测Fas/Fas L的表达，并研究其是否诱导Jurkat T淋巴细胞凋亡。细胞因子预处理（LPS, TNF-a, IL-1b, IL-8）的效果也被检测。未刺激的II型细胞同时表达Fas/Fas L及其mRNA，细胞因子预处理（LPS<TNF-a<IL-8<IL-1b）增强了Fas/Fas L及其mRNA的表达。与未刺激的II型细胞共培养后，5%的Jurkat细胞发生凋亡，细胞因子预处理（LPS 8%, TNF-a 17.5%, IL-1b 20%, IL-8 22%）显著增加凋亡频率。NOK-1预处理可抑制细胞因子诱导的Jurkat细胞凋亡增加80%。这些结果表明，细胞因子刺激的II型细胞诱导Fas阳性Jurkat T淋巴细胞凋亡，并且Fas/Fas L系统特异性参与了这一过程。少

1. Expression of Fas/Fas ligand in human acute respiratory distress syndrome (ARDS) and induction of apoptosis in T lymphocyte.We examined expression of Fas/Fas ligand (Fas L) in 27 human ARDS autopsy lungs, and determined if it induced apoptosis in Fas-positive Jurkat T lymphocytes. Fas was detected in all the phases of ARDS lungs, whereas Fas L was expressed on alveolar epithelium in the acute phase of ARDS lungs, which decreased in the hyaline membrane and proliferative phases of ARDS. The sections from ARDS lungs induced apoptosis in Jurkat T lymphocytes, frequency of which was highest in the acute phase of ARDS and decreased in the hyaline membrane and proliferative phases of ARDS. This apoptosis in Jurkat T lymphocytes was almost completely inhibited by pretreatment with NOK-1. These results suggested that expression of Fas L in alveolar epithelium played a role in protecting the lung from injury by inducing apoptosis in pro-inflammatory cells such as lymphocytes.2. Expression of … More Fas/Pas ligand in rat isolated pulmonary alveolar type II cells and induction of apoptosis in T lymphocyte.We examined expression of Fas/Fas L in rat isolated pulmonary alveolar type II cells (type II cells), and investigated if it induced apoptosis in Jurkat T lymphocytes. The effect of pretreatment with cytokines (LPS, TNF-a, IL-1b, IL-8) was also examined. Unstimulated type II cells expressed both Fas/Fas L and their mRNA, which were enhanced by pretreatment with cytokines (LPS<TNF-a<IL-8<IL-1b). Five % of Jurkat cells underwent apoptosis after co-cultured with unstimulated type II cells, and the frequency of apoptosis was significantly increased by pretreatment with cytokines (LPS 8 %, TNF-a 17.5 %, IL-1b 20 %, IL-8 22 %). Pretreatment with NOK-1 inhibited cytokine-induced increase of apoptosis in Jurkat cells by 80 %. These results suggested that cytokine-stimulated type II cells induced apoptosis in Fas-positive Jurkat T lymphocytes, and the Fas/Fas L system was specifically involved in this process. Less