Finally, since we demonstrated that infection with wild-type H. pylori strain 7.13 induced significantly higher levels of inflammation and injury compared to infection with the cagA isogenic mutant (Fig. 1B to I), we next compared the gastric microbiota of gerbils infected with wild-type H. pylori strain 7.13 (n = 7) that harbored relatively low levels of gastric inflammation (inflammation scores of 0 or 1) to gerbils infected with the cagA isogenic mutant (n = 11) to determine the potential role of inflammation in cagA-dependent gastric dysbiosis (Fig. 2E). This evidence concerns the gene S100A8 and infection.