@Article {Comer1058，作者= {Comer，David M.和Nedney，Joseph C.和Ennis，Madeleine and Madeleine和Elborn，J。Stuart}，Title = {Copd，Smoker and nonsmokers in airway上皮细胞凋亡和炎症{41}，number = {5}，页= {1058--1067}，年= {2013}，doi = {10.1183/09031936.00063112}，publisher = {欧洲呼吸社会}188bet官网地址慢性阻塞性肺疾病（COPD）的细胞（PBEC）对烟雾提取物（CSE）暴露后的铜绿假单胞菌（LPS）的反应不同于与从没有气流阻塞和非吸烟者的吸烟者获得的PBEC相比。来自16名COPD受试者的PBEC，10名没有气流阻塞的吸烟者，在空气{\ textendandash}液体界面上培养了9名非吸烟者。在用铜绿假单胞菌LPS刺激之前，将培养物与CSE孵育。通过ELISA和TOLL样受体（TLR）-4通过荧光激活的细胞分散剂来测量白介素（IL）-6和IL-8。核因子（NF）-κB的激活是通过蛋白质印迹和ELISA确定的，MAPK和CASPASE-3活性通过蛋白质印迹。使用膜联蛋白-V染色和末端转移酶介导的DUTP NICT端鉴定方法评估凋亡。IL-8和IL-6的本构释放是COPD培养物中最大的。然而，CSE预处理后面是铜绿假单胞菌LPS刺激降低了COPD PBEC的IL-8释放，但它是从没有气流阻塞和非吸烟者的吸烟者细胞中增加的。 TLR-4 expression, MAPK and NF-κB activation in COPD cultures were reduced after CSE treatment, but not in the smokers without airflow obstruction or nonsmoker groups, which was associated with increased apoptosis. CSE attenuates inflammatory responses to LPS in cells from people with COPD but not those from nonsmoking individuals and those who smoke without airflow obstruction.}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/41/5/1058}, eprint = {//www.qdcxjkg.com/content/41/5/1058.full.pdf}, journal = {European Respiratory Journal} }