Vitamin C-deficient gulo-/- mice exhibit increased susceptibility to Helicobacter pylori colonization and gastric pathology.

Low dietary intake of vitamin C (ascorbic acid) has been associated with unfavorable clinical outcomes of Helicobacter pylori infection in human studies. However, experimental evidence regarding the influence of host vitamin C status on H. pylori colonization remains inconsistent across animal models. In this study, we generated vitamin C-deficient L-gulono-γ-lactone oxidase-deficient (gulo-/-) mice on an FVB genetic background to evaluate host susceptibility to H. pylori infection under defined vitamin C supplementation conditions. FVB gulo-/- mice were orally infected with H. pylori and provided drinking water containing either low (330 mg/L) or high (3300 mg/L) concentrations of vitamin C. Gastric colonization levels were assessed at 16 and 32 weeks post-infection (WPI). At 16 WPI, H. pylori colonization was significantly higher in gulo-/- mice receiving low-dose vitamin C compared with those receiving high-dose supplementation (p = 0.007) and wild-type mice (p = 0.03). Histopathological analysis revealed increased lymphocytic infiltration in the gastric mucosa of gulo-/- mice receiving low-dose vitamin C during chronic infection, whereas minimal inflammatory changes were observed in mice receiving high-dose vitamin C. These findings demonstrate that vitamin C deficiency influences H. pylori colonization and gastric pathology in a host genetic background-dependent manner. The FVB gulo-/- mouse model provides a useful experimental platform for investigating host factors that modulate H. pylori infection and disease progression.