Abstract

This research was to investigate the difference of hepatic histopathology and apoptosis between the diet-induced obesity (DIO) and normal (lean) mice after Escherichia coli (E. coli) pneumonia. A total of 128 ICR mice were selected to be challenged intranasally with phosphate-buffered saline (PBS) or 4×109CFUs/mL of E. coli, and the liver histopathology and apoptosis were examined pre- and post-infection. Results showed that the liver index, levels of lipid droplets, cytokines, adipocytokines, oxidative stress, apoptotic percentage, and apoptotic related factors in the E. coli-infected mice were generally higher than those in the uninfected mice, whereas the hepatic glycogen and Bcl-2 were the opposite. Interestingly, after E. coli infection, the DIO-E. coli mice exhibited decreased liver index and apoptotic percentages, and reduced levels of TNF-α, IL-6, resistin, MDA, GSH, CAT, Caspase-3, Caspase-9, Bax as well as Bax/Bcl-2 ratio in comparison to the lean-E. coli mice. Our results indicated that E. coli-induced pneumonia caused hepatic histopathological damage, increased hepatic apoptosis, oxidative damages, and higher levels of cytokines and adipocytokines. However, such changes showed less severely in the DIO mice than in the lean mice following E. coli pneumonia.

Highlights

  • Obesity, defined as a state of abnormal or excessive accumulation of adipose tissue due to imbalance in energy consumption and expenditure, increases the risk of various metabolic disease, such as type II diabetes, cardiovascular diseases and steatohepatitis [1]

  • Before pulmonary E. coli infection, the liver weight in the diet-induced obesity (DIO) group was higher (p0.05)

  • Corrales-Medina and colleagues found that obesity may exert a protective effect against 30-day mortality from communityacquired bacterial pneumonia [20]

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Summary

Introduction

Obesity, defined as a state of abnormal or excessive accumulation of adipose tissue due to imbalance in energy consumption and expenditure, increases the risk of various metabolic disease, such as type II diabetes, cardiovascular diseases and steatohepatitis [1]. The term “obesity paradox” was coined by Gruberg and colleagues who found that obese patients (BMI ≥ 30kg/m2) had lower risk for the in-hospital complications and one-year mortality rates after percutaneous coronary intervention compared with normal-weight (18.5 ≤ BMI ≤ 25 kg/m2) [12]. The infection-induced lipid metabolic disorders were slighter in the DIO mice than in the lean mice through AMPKα pathway in the state of non-fatal pneumonia caused by instillation E. coli [16]

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