Obesity has developed into a considerable health problem in the whole world. Escherichia coli (E. coli) can cause nosocomial pneumonia and induce cell apoptosis during injury and infection. Normal (lean) and diet-induced obesity mice (DIO, fed with high-fat diet) were chosen to perform nasal instillation with E. coli to establish a nonfatal acute pneumonia model. At 0 h, 12 h, 24 h, and 72 h postinfection, lung tissues were obtained to measure cell apoptosis. As shown in this study, both lean and DIO mice exhibited histopathological lesions of acute pneumonia and increased cell apoptosis in the lung infected with E. coli. Interestingly, the relative mRNA and protein expressions associated with either endoplasmic reticulum stress or death receptor apoptotic pathway were all dramatically increased in the DIO mice after infection, while only significant upregulation of death receptor apoptotic pathway in the lean mice at 72 h. These results indicated that the DIO mice executed excess cell apoptosis in the nonfatal acute pneumonia induced by E. coli infection through endoplasmic reticulum stress and death receptor apoptotic pathway.

中文翻译：

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饮食诱导的肥胖小鼠在大肠杆菌感染后通过死亡受体和ER应力途径执行肺细胞凋亡。

肥胖已发展成为全世界相当大的健康问题。大肠杆菌（E. coli）可以引起医院内肺炎，并在损伤和感染过程中诱导细胞凋亡。选择正常（瘦）和饮食诱发的肥胖小鼠（DIO，用高脂饮食喂养）通过大肠杆菌进行鼻内滴注，以建立非致死性急性肺炎模型。在感染后0、12、24和72小时，获得肺组织以测量细胞凋亡。如本研究所示，瘦小鼠和DIO小鼠均表现出急性肺炎的组织病理学损害，并在受大肠杆菌感染的肺部细胞凋亡增加。有趣的是，感染后，DIO小鼠中与内质网应激或死亡受体凋亡途径相关的相对mRNA和蛋白质表达均显着增加，而瘦小鼠在72 h时死亡受体凋亡途径仅显着上调。这些结果表明，DIO小鼠通过内质网应激和死亡受体凋亡途径，在大肠杆菌感染引起的非致死性急性肺炎中执行了过量的细胞凋亡。