Fig. 5: Loss of lctP renders H. pylori colonization deficient in a manner that is recovered by loss of complement.

a Two-weeks infection by H. pylori strains. Group of C57BL/6J WT (n = 8) and isogenic C3−/− (n = 8) mice were infected with the H. pylori PMSS1 WT; another group of C57BL/6J WT (n = 6) and isogenic C3−/− (n = 6) mice were infected with the ΔlctP strain. b One-year infection by H. pylori strains. Group of C57BL/6J WT (n = 4) and isogenic C3−/− (n = 3) mice were infected with the H. pylori PMSS1 WT; another group of C57BL/6J WT (n = 4) and isogenic C3−/− (n = 4) mice were infected with the ΔlctP strain. The WT and C3−/− mice were cohoused at weaning for at least 4-weeks before the infection and remained cohoused for the whole experimental period. At the indicated time points, the stomachs were collected and bacterial CFUs were determined by plating. Each point represents one mouse sample, with black bars representing the mean. Gray dotted line represents the limit of detection. The p values were obtained by Tukey’s multiple comparisons test. The significance was indicated as * (p < 0.05), ** (p < 0.01), and n.s. (no significance). Source data and exact p values are provided in the Source Data file.