<i>Gli1</i> deletion prevents gastric metaplasia.

<p>A) Schematic representation of LacZ substitution for the Gli1 gene to generate Gli1^+/− and Gli1^−/− mice. B) Gli1 mRNA in stomachs of WT, Gli1^+/− and Gli1^−/− mice. C) Stomach weight normalized to total body weight in infected and uninfected mice. D) Triple immunofluorescent staining of <i>Griffonia simplicifolia</i> II (GSII) lectin (green; mucous neck cells), intrinsic factor (red; chief cells), and H⁺/K⁺-ATPase (orange; parietal cells) in 6-month <i>H. felis</i>-infected WT, Gli1^+/− and Gli1^−/− stomachs. E) Hematoxylin and eosin (H&E) staining of the gastric mucosa in 6-month <i>H. felis</i>-infected WT, Gli1^+/− and Gli1^−/−. F–H) Histologic scoring of metaplasia, PMN infiltration, and displacement of epithelial glands by infiltrating inflammatory cells in 2- and 6-month <i>H. felis</i>-infected WT, Gli1^+/− and Gli1^−/− stomachs. I) qPCR quantification of <i>H. felis</i> flagellar filament B (Fla-B) DNA in the infected mucosa. J) Flow cytometric analysis of F4/80⁺ cells versus side-scatter in WT Sham and 6-month infected WT, Gli1^+/− and Gli1^−/− stomachs (N = 3 mice per group). Open and closed bars denote uninfected and infected mice respectively. For RT-qPCR experiments, N = 5–10 mice per group. Error bars represent the mean +/− SEM. ***p<0.001; **p<0.01; *p<0.05. N.S. = not significant.