Abstract

Obese mice presented lower mortality to non-fatal pneumonia induced by Escherichia coli (E. coli) than the non-obese mice. However, it remained obscure whether the intestine contributed to the protective effect of obese mice with infection. The 64 non-obese (NOB) mice were divided into NOB-uninfected and NOB-E. coli groups, while 64 high-fat diet-induced obesity (DIO) mice were divided into DIO-uninfected and DIO-E. coli groups. Mice in E. coli groups were intranasally instilled with 40 μl E. coli (4.0 ×109 colony-forming units [CFUs]), while uninfected groups with the same volume of phosphate buffer saline (PBS). The T subsets of Intraepithelial lymphocytes (IELs) and lamina propria lymphocytes (LPLs) in the intestine were collected for flow cytometry analysis at 0, 12, 24, and 72 h post-infection, also the duodenum and colon were harvested to survey histopathological change. The results showed that the percentage of CD3+T cells in LPLs in DIO-E. coli group was significantly lower than that in the DIO-uninfected group after infection (p < 0.05). The percentage of CD4+T cells in IELs in NOB-E. coli was significantly lower than that in DIO-E. coli after infection (p < 0.05). The percentage of CD8+T cells in LPLs in NOB-E. coli was significantly lower than that in DIO-E. coli at 12 and 24 h (p < 0.05). The immunoglobulin A (IgA)+ cells in DIO-uninfected were higher than that in NOB-uninfected at all time points (p < 0.05). The IgA+ cells in DIO-E. coli were higher than that in DIO-uninfected at 12, 24, and 72 h (p < 0.05). The results revealed that the level of intestinal mucosal immunity in obese mice was more active than that in non-obese mice.

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