Animal models Characterization of symptoms in diabetic mice Infection route or sepsis induction Cellular or molecular observation in diabetic mice with sepsis Reference
STZ (140 mg/kg)-induced diabetes in CF1 mice (T1D) with P. aeruginosa(NC-5 strain) infection No increase in acute death rate. Increase in the number of bacteria in kidney, liver, spleen and peripheral blood. Intravenous injection (i) Less effect of pass protection in immune serum from diabetic vaccinated mice in normal recipients, implying the impairment of antibody- or cytokine-mediated immunity.
(ii) Less effect of protection in immune serum from normal vaccinated mice into diabetic recipients, implying the impairment of immune cells-mediated immunity
STZ (50 mg/kg for 5 consecutive days)-induced diabetes in CD-1 mice (T1D) with type VI GBS (NCTC 1/82 strain) infection Lower 50% lethal dose (>1 log10 in CFU). Increase in bacterial growth in blood and kidney. Intravenous
Increase in IL-6, IL-1b, IL-10, TNF-a and decrease in IFN-glevels in the serum of diabetic mice with sepsis. [42]
GotoKakizaki (GK) rats (T2D) with CLP Not validated CLP-induced sepsis Increase in plasma lactate, IL-6 and IL-10 20 hr after CLP in diabetic mice with sepsis [44]
AKITA mice (T1D) with CLP Increase in the sepsis-induced mortality CLP-induced sepsis (i) Greater number of circulating neutrophils at first 24hr after CLP in diabetic mice.
(ii) Decrease in pro-inflammatory and anti-inflammatory cytokines in diabetic mice compared with died mice.
Table 2: Comparison of the characteristics and immune dysfunction in diabetic mouse models of sepsis.