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. 2020 Apr 14;9(4):959. doi: 10.3390/cells9040959

Figure 8.

Figure 8

Deficiency of IL-18 increases intestinal permeability and accelerates Type 1 diabetes onset. The WT and IL-18−/− mice were injected with STZ (40 mg/kg) or a vehicle solution (VH, non-diabetic, 0 days after STZ) for five consecutive days, and the clinical parameters were evaluated. (A) The incidence of diabetes. (B) The blood glucose levels in the WT and IL-18−/− mice at 0, 7 and 15 days after the vehicle or STZ injections. (C) The insulin levels, assessed by ELISA, in the serum of the WT and IL-18−/− mice at 15 days after the vehicle or STZ injections. (D) The score of inflammatory infiltrates in the islets of the WT and IL-18−/− mice at 15 days after the vehicle or STZ injections. (E) Histopathology of the pancreatic tissue of the WT and IL-18−/− mice at 15 days after the STZ injections. (F) The 16S rRNA gene expression in the PLNs of the WT and IL-18−/− mice at 15 days after the STZ injection. (G) The FITC-Dextran levels in the serum of the WT and the IL-18−/− mice at 15 days after the STZ or vehicle injections. (H–L) The gene expression of ZO-1, claudin-2, Occludin and RegIIIy, respectively, in the ileum of the WT and IL-18−/− mice at 15 days after the STZ induction. The values are expressed as the mean ± SD. The results were considered statistically significant when p < 0.05 (*; #, ∞). N = 3–6 animals per group. Significant differences between the groups were determined by one-way ANOVA, followed by Tukey’s multiple-comparison test.