Fig. 1.

CagA⁺ H. pylori infection exacerbates DSS-induced chronic colitis in mice. A Schematic depiction of the experimental design for H. pylori (CagA⁺ strain) inoculation followed by chronic colitis models administrated 2% DSS. B, C Body weights (B) and disease activity index (DAI) changes (C) in different groups. Data from the second and third DSS-treatment cycles (7 day 2% DSS and 7 day diluted water) showed that H. pylori-infected mice had significantly less body weight loss and disease manifestation than control mice with no H. pylori infection in DSS-treated conditions. ***p < 0.001, compared to DSS group. Student’s t test for body weights, and χ² test for DAI scores. D, E, F Colon lengths (D), spleen weights (E), microscopic appearance and H&E histological sections of the colon F in each group. Scale bars, 200 µm (200 ×) and 100 µm (400 ×). **p < 0.01, ***p < 0.001. Student’s t test was used for colon length and spleen weights, and the χ² test was used for histological scores. G The relative expression of tight junction proteins (TJs) in the colon of H. pylori and chronic colitis mice. The augmented Claudin-2 was observed in the H. pylori + DSS group in comparison with the DSS group. H The TJs protein expression of chronic colitis mice subgroups without H. pylori, with CagA⁻ H. pylori infection, and with CagA⁺ H. pylori infection. Claudin-2 was significantly upregulated in CagA⁺ H. pylori-infected group compared with CagA⁻ H. pylori mice. All data were presented as means ± SD (n = 10)