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Interleukin-17 receptor B (IL-17RB), a member of the IL-17 receptor family activated by IL-17B/IL-17E, has been shown to be involved in inflammatory diseases. However, the regulation and function of IL-17RB in  Helicobacter pylori  ( H. pylori ) infection, especially in the early-phase is still unknown. Here, we found that gastric IL-17RB mRNA and protein were decreased in gastric mucosa of both patients and mice infected with  H. pylori . In vitro experiments show that IL-17RB expression was down regulated via PI3K/AKT pathway on gastric epithelial cells (GECs) stimulated with  H. pylori  in a  cagA -involved manner, while in vivo studies showed that the effect was partially dependent on  cagA  expression. IL-17E was also decreased during the early-phase of  H. pylori  infection, and provision of exogenous IL-17E resulted in increased CD11b + CD11c −  myeloid cells accumulation and decreased bacteria colonization within the gastric mucosa. In the early-phase of  H. pylori  infection, IL-17E-IL-17RB promoted gastric epithelial cell-derived CXCL1/2/5/6 to attract CD11b + CD11c −  myeloid cells, and also contributed to host defense by promoting the production of antibacterial protein Reg3a. This study defines a negative regulatory network involving IL-17E, GECs, IL-17RB, CD11b + CD11c −  myeloid cells, and Reg3a in the early-phase of  H. pylori  infection, which results in an impaired host defense within the gastric microenvironment, suggesting IL-17RB as a potential early intervening target in  H. pylori  infection.

cell death and disease

Decreased IL-17RB expression impairs CD11b+CD11c− myeloid cell accumulation in gastric mucosa and host defense during the early-phase of Helicobacter pylori infection