Why the study?
Obesity is a risk factor for many diseases but may benefit individuals with bacterial infection, leading researchers to investigate the relationship between obesity and the heart during nonfatal bacterial infection.
Does diet-induced obesity attenuate cardiac injury during nonfatal E. coli infection in mice?
Does diet-induced obesity attenuate cardiac injury during nonfatal E. coli infection in mice?
In a mouse model of nonfatal E. coli infection, diet-induced obesity paradoxically attenuated cardiac inflammation, oxidative stress, and apoptosis compared to lean controls.
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Caution against clinical extrapolation; leaves open obesity paradox in infection-related cardiac injury.
Obesity is a risk factor of many diseases, but could be beneficial to the individuals with bacterial infection. The present study was conducted to investigate the relationship between obesity and heart during nonfatal bacterial infection. Male 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 mouse model. The cardiac histopathology, inflammation and oxidative damage, as well as apoptosis were detected post-infection. The results revealed that the Escherichia coli (E.coli)-infected mice exhibited increased cardiac index, contents of IL-1β, IL-6, IL-8, TNF-α, leptin and resistin, levels of apoptotic proteins (caspase-3 and caspase-9, and bax/bcl-2 ratio), cardiac pathological changes and oxidative stress. Furthermore, these parameters were more serious in the lean mice than those in the DIO mice. In summary, our findings gave a new sight that E.coli infection impaired heart via histopathological lesions, inflammation and oxidative stress and excessive apoptosis of cardiomyocytes. Interestingly, obesity exerted attenuated effects on the heart of mice with non-fatal infection of E.coli through decreased inflammation, oxidative stress and apoptosis of cardiac tissue.
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Guo et al. (2021) studied this question.
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