Abstract
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.
Highlights
Pneumonia has been recognized as a common cause of sepsis in critically ill patients today [1]
Neutrophils are the first circulating leukocytes to respond during E. coli pneumonia [8], and its apoptosis after killing pathogen is considered to be essential for the downregulation of inflammatory response [9]
In conditions of prolonged stress, oxidative stress may have an interaction with endoplasmic reticulum stress, and influence unfolded protein
Summary
Pneumonia has been recognized as a common cause of sepsis in critically ill patients today [1]. More than 60% of nosocomial pneumonias are caused by gram-negative enteric bacilli [2]. Escherichia coli (E. coli), a rod-shaped gram-negative bacterium, could produce disease of organ systems other than the gut, including urinary tract infection, meningitis, septicemia, severe community-, and ventilator-acquired pneumonia in humans and animals [3,4,5,6]. Innate immune responses initiate the release of proinflammatory cytokines and recruitment of inflammatory cells [7]. Neutrophils are the first circulating leukocytes to respond during E. coli pneumonia [8], and its apoptosis after killing pathogen is considered to be essential for the downregulation of inflammatory response [9]. TNF-α, a major extrinsic mediator of apoptosis, is a cytokine produced mainly by activated macrophages. TNF-related apoptosis plays an important role in the orchestration of the innate immune responses [12]. In conditions of prolonged stress, oxidative stress may have an interaction with endoplasmic reticulum stress, and influence unfolded protein
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