Histopathological Changes Caused by Inflammation and Oxidative Stress in Diet-Induced-Obese Mouse following Experimental Lung Injury

Abstract

Obesity has been identified as a risk factor for adverse outcomes of various diseases. However, information regarding the difference between the response of obese and normal subjects to pulmonary inflammation is limited. Mice were fed with the control or high-fat diet to establish the lean and diet-induced obese (DIO) mice. Escherichia coli was intranasally instilled to reproduce non-fatal acute pneumonia model. After infection, serum samples and lung tissues were obtained at 0, 12, 24, and 72 h. DIO mice exhibited increased serum triglyceride (TG) and total cholesterol (TC) contents as well as pulmonary resistin, IL-6, and leptin levels compared with lean mice. E. coli infection caused an acute suppurative inflammation in the lung with increased lung index and serum TG and TC contents; elevated pulmonary tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8, and leptin levels; and oxidative stress in mice. Interestingly, almost all the above-mentioned parameters peaked at 12 h after infection in the lean-E. coli group but after 12 h in the DIO-E. coli group. These results indicated that the DIO mice presented a delayed inflammatory response and oxidative stress in non-fatal acute pneumonia induced by E. coli infection.

RETRACTED ARTICLE: Effect of intranasal instillation of Escherichia coli on apoptosis of spleen cells in diet-induced-obese mice

“…Mice from Lean-E. coli and DIO-E. coli groups underwent intranasal instillation with 40 μL of a suspension containing ~10 9 CFU of E. coli. Mice from Lean-PBS and DIO-PBS groups were given the same dose of PBS 4,5 . Two mice which died within 6 h of intranasal instillation were removed.…”

“…Interestingly, recent studies have shown that obesity played a protective part in pneumonia 4,5 . Preliminary study of Gu reported that obesity could alleviate oxidative damage and inflammation of mice spleen under the condition of non-fatal acute pneumonia induced by Escherichia coli 6 .…”

Obesity Enhances Antioxidant Capacity and Reduces Cytokine Levels of the Spleen in Mice to Resist Splenic Injury Challenged by Escherichia coli

“…Obesity is growing rapidly around the world, and the diseases associated with obesity have been highlighted in recent years, especially pulmonary disease. Recently, studies suggested that obesity plays a beneficial role in E. coli pneumonia, manifesting that clinically significant changes in pulmonary inflammatory response may be associated with immune status in obesity [4,5]. The spleen is the center of cellular immunity and humoral immunity.…”

“…Fascinatingly, 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. The DIO mice also presented a delayed pulmonary inflammatory response and oxidative stress in pneumonia induced by E. coli infection [5]. In addition, 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].…”

“…Additionally, serum triglyceride and total cholesterol contents (A110-1 and A111-1, Nanjing Jiancheng Bioengineering Institute, China) were examined. The mice in N-E. coli and DIO-E. coli were anesthetized with ether and challenged intranasally with 40 μL of bacterial suspension containing approximately 10 9 CFUs of E. coli which was provided by the Veterinary Medical Laboratory of Sichuan Agricultural University (Chengdu, China) as described previously [4,5]. And the same dose of PBS was given to the mice in N-PBS and DIO-PBS by the same method.…”