Abstract
Obese mice exhibited more lymphocytes in the bronchoalveolar lavage fluid and milder lung injury after Escherichia coli (E. coli) infection. However, it remained unclear whether the spleen contributed to the effect of obese mice with infection. The study was purposed to reveal the histopathological changes of the spleen caused by oxidative stress and inflammation in diet-induced obesity (DIO) mice challenged by Escherichia coli. After infection, the spleen tissues were obtained in normal and DIO mice at 0 h (uninfected), 12 h, 24 h, and 72 h postinfection. Results revealed that DIO mice have higher contents of resistin, TNF-α, IL-6, and IL-1β in the spleen than normal mice and lower concentrations of GSH-Px, SOD, and CAT and higher MDA than normal mice. After an intranasal drip of E. coli, the activities of GSH-Px, SOD, and CAT in the DIO mice were elevated and the content of MDA declined. The activities of SOD and CAT in the normal mice declined, and the content of MDA was elevated. Moreover, the contents of TNF-α, IL-6, and IL-1β in the spleen declined in DIO mice at 24 and 72 h, although the contents of leptin, resistin, TNF-α, IL-6, and IL-1β were elevated at 12 h. The contents of resistin, TNF-α, IL-6, and IL-1β were elevated in normal mice at 12 and 24 h. Those results indicated that obesity elevated splenic oxidation and inflammatory levels, but it enhanced antioxidant capacity and reduced cytokine levels of the spleen in mice to resist splenic injury after an intranasal drip of E. coli.
Highlights
Obesity is a complex chronic disorder with multifactorial etiology, involving genetics, hormones, diet, and environments [1]
Wan et al [4] have reported that the obese mice exhibited more lymphocytes in the bronchoalveolar lavage fluid and milder lung injury than normal mice under the case of nonfatal pneumonia caused by E. coli, suggesting that obesity can improve immune responses against bacterial pneumonia
There were no significant changes in the mental status, feeding status, and activity status of the mice in N-PBS and diet-induced obesity (DIO)-PBS groups
Summary
Obesity is a complex chronic disorder with multifactorial etiology, involving genetics, hormones, diet, and environments [1]. Emerging data indicated that obesity is closely related to infectious diseases and obesity increased susceptibility to bacterial infections [2]. Obesity was recognized as a significant risk factor for pneumonia with increased incidence and severity of disease [3]. The DIO mice presented a delayed pulmonary inflammatory response and oxidative stress in pneumonia induced by E. coli infection [5]. The previous study found that the changes of hepatic histopathological damage, oxidative damage, and higher levels of cytokines (TNF-α, IL-6, and resistin) showed to be less severe in the DIO mice than in the normal mice following E. coli pneumonia [6].
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