CXCL3 and gastritis: This not only led to decreased E-cadherin and ZO-1 by MMP1, thereby promoting gastric mucosal damage to foster H. pylori colonization, but also resulted in increased gastric influx of G-MDSCs via CXCL3-dependent migration, thereby promoting gastritis and impairing H. pylori-specific IFN-γ-producing CD4+ T cell responses to foster H. pylori colonization.