Fig. 4: Exogenous IL-17E inhibits bacterial colonization and induces CD11b+CD11c− myeloid cell accumulation in gastric mucosa during the early-phase of H. pylori infection.

a The bacterial colonization in gastric mucosa of WT H. pylori-infected mice injected with IL-17B, IL-17E, IL-17B, and IL-17E, or PBS control on day 9 p.i. was compared. Each dot represents one mouse. (b and c) The percentages of CD11b+CD11c− myeloid cells among CD45+ cells in blood (b) or gastric mucosa (c) of uninfected mice and WT H. pylori-infected mice injected with IL-17B, IL-17E, IL-17B, and IL-17E, or PBS control on day 9 p.i. were compared. Each dot represents one mouse. d Representative dot plots of CD11b+CD11c− myeloid cells by gating on CD45+ cells in gastric mucosa of uninfected mice and WT H. pylori-infected mice injected with IL-17B, IL-17E, IL-17B, and IL-17E, or PBS control on day 9 p.i. Numbers indicate relative percentages among CD45+ cells. e Surface expression of F4/80 and Ly6G on CD11b+CD11c− myeloid cells by gating on CD45+ cells in gastric mucosa of WT H. pylori-infected mice on day 9 p.i. as analyzed by flow cytometry. f Wright staining of sorted peripheral blood CD11b+CD11c- myeloid cells from H. pylori-infected patients. *P < 0.05, **P < 0.01, n.s. P > 0.05 for groups connected by horizontal lines compared