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. 2022 Jun 15;14(3):567–586. doi: 10.1016/j.jcmgh.2022.06.002

Figure 7.

Figure 7

TLR9 is up-regulated in human H pylori-infected and mouse H felis-infected gastric tissues, and H felis-induced gastric hyperplasia is suppressed in TLR9-deficient mice. (A and B) Gene expression of TLR9 in gastric tumors from (A) TCGA intestinal-type GC patients (Hp-, n = 53; Hp+, n = 4), and (B) Australian/Chinese GC patients (Hp-, n = 13; Hp+, n = 7), based on their H pylori (Hp) status. ∗P < .05; unpaired Student t test. (C) qPCR expression of TLR9 (relative to 18S rRNA) in gastric tissues from GC-free individuals, based on the H pylori status (Hp- normal (N), n = 8; Hp- mild gastritis (M), n = 12; Hp- severe gastritis (S), n = 8; total Hp-, n = 28; Hp+ severe gastritis (S), n = 11). ∗∗P < .01; one-way ANOVA. (D) qPCR expression of Tlr9 (relative to 18s rRNA) in gastric body tissues from WT mice at 4 months after oral gavage with either broth or H felis (Hf). n = 6 mice/group. ∗∗P < .01; unpaired Student t test. (E and F) Shown are (E) stomach weights and (F) mucosal thicknesses of WT and Tlr9-/- mice at 4 months after oral gavage with either broth or H felis (n = 12 mice/group). (G) Representative photomicrographs showing H&E-stained whole slide scans of stomachs. Scale bars: 1 mm. (H) Western blots of gastric body tissue lysates from Tlr9-/- and WT mice at 4 months after oral gavage with either broth or H felis with the indicated antibodies. Graphs depict densitometry quantification of the indicated phosphorylated signaling molecules shown in the Western blots (n = 3 lysates/group), and relative expression was determined against the corresponding amount of total protein. ∗P < .05, ∗∗P < .01; one-way ANOVA.