Pulmonary alveolar epithelium protects the lung through apoptosis of T lymphocytes

1.为探讨Fas/Fas配体（Fas/Fas L）在人急性呼吸窘迫综合征（ARDS）中的表达及诱导T淋巴细胞凋亡的作用，我们检测了27例ARDS尸检肺组织中Fas/Fas L的表达，并检测了Fas L是否诱导Fas阳性Jurkat T淋巴细胞凋亡。Fas在ARDS各期肺组织中均有表达，而Fas L在ARDS急性期肺泡上皮细胞表达，在ARDS肺透明膜期和增殖期表达减弱。从ARDS肺切片诱导Jurkat T淋巴细胞凋亡，其频率在ARDS急性期最高，并在ARDS的透明膜和增殖期下降。用NOK-1预处理几乎完全抑制Jurkat T淋巴细胞的这种凋亡。提示肺泡上皮细胞Fas L的表达可能通过诱导淋巴细胞等促炎细胞凋亡而发挥肺保护作用.表达 ...更多信息 Fas/Pas L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检测了Fas/Pas L在大鼠肺泡Ⅱ型细胞（Ⅱ型细胞）中的表达，并探讨了Fas/Pas L是否诱导Jurkat T淋巴细胞凋亡。用细胞因子（LPS、TNF-α、IL-1b、IL-8）预处理也检查了效果。未受刺激的Ⅱ型细胞表达Fas/Fas L及其mRNA，经细胞因子预处理（LPS<TNF-α <IL-8<IL-1b）后表达增强。与未经刺激的Ⅱ型细胞共培养后，Jurkat细胞凋亡率为5%，经细胞因子（LPS 8%、TNF-α 17.5%、IL-1b 20%、IL-8 22%）预处理后，凋亡率明显增加。用NOK-1预处理抑制了80%的姜黄素诱导的Jurkat细胞凋亡的增加。这些结果表明，苦参碱刺激的II型细胞诱导Fas阳性的Jurkat T淋巴细胞的凋亡，Fas/Fas L系统是专门参与这一过程。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