| 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 |
[41] |
| 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
injection |
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. |
[43] |
