Here, we have shown, for the first time, that infection with H. pylori elevates host ANGPTL4 expression, which reshapes the gastric environment by promoting the infiltration of mononuclear cells (Tregs in our data) rather than granulocytes (neutrophils in our data) into the infected gastric mucosa, directly leading to gastritis progression and bacterial persistence. Here, ANGPTL4 is linked to infection.