Figure 2.

Helicobacter pylori induces proliferation in gastroids via CagA and β-catenin. (A and B) Gastroids were infected with wild-type (WT) H.pylori strain 7.13 or an isogenic 7.13 cagA⁻ null mutant (red) via luminal microinjection and proliferation was quantified using 5-ethynyl-2′-deoxyuridine (EdU) (green). (A) Representative staining in uninfected (left panel), WT H. pylori-infected (middle panel) or H. pylori cagA⁻ mutant-infected (right panel) gastroids. (B) EdU quantification demonstrating increased proliferation in WT H. pylori infected gastroids. (C and D) Gastroids were pretreated with cardionogen 1, a β-catenin inhibitor (i), and then infected with H. pylori and proliferation was quantified by EdU. (C) Representative staining in uninfected or WT H. pylori-infected gastroids, with or without pretreatment with cardionogen 1. (D) EdU quantification demonstrating that increased proliferation in H. pylori WT-infected gastroids is abolished by pretreatment with cardionogen 1. Data are expressed as means±SEM, n=3 independent replicates.