Abstract
The incidence of Klebsiella pneumoniae liver abscess (KPLA) has increased in a number of Asian countries over the past 30 years. Diabetes mellitus (DM) is a risk factor for KPLA. The prevalence and clinical features of KPLA in patients with and without DM have been well described; however, the underlying molecular mechanism responsible for the increased incidence of KPLA in patients with DM remains unclear. In the present study, a mouse model of DM was constructed and mice were infected with K. pneumoniae. Tissues were harvested for immunohistochemical and inflammatory factor expression analyses. The results revealed that the number of liver abscesses in mice with DM was greater than that observed in normal mice. The expression of interleukin (IL)-1β, IL-2, IL-6, macrophage inflammatory protein-1α and tumor necrosis factor-α in the liver tissues of mice with DM was significantly higher compared with normal mice. Western blotting results revealed that the expression of phosphorylated (p)-inhibitor of nuclear factor κB (NFκB) kinase subunit β, p-NFκB and p-inhibitor of NFκB was significantly increased in the liver tissue of mice with DM compared with that of normal mice. These results suggest that activation of the NFκB signaling pathways has a regulatory effect on the pathogenesis of K. pneumoniae bacteria liver abscesses and that high glucose conditions may promote the activation of NFκB signaling.