In vitro infection of different cell types by H. pylori revealed that HPnc4160/NikS decreases CagA-dependent bacterial internalization, reduces cell colonization and epithelial barrier disruption (Eisenbart et al., 2020) and also decreases the level of phosphorylated CagA, IL8 production and the associated CagA-induced hummingbird phenotype (Kinoshita-Daitoku et al., 2021). Here, S100A8 is linked to infection.