FIG. 3.

Innate immune recognition of H. pylori. Innate immune recognition of H. pylori leads to production of proinflammatory cytokines by macrophages (Mφ), DCs, mast cells, and gastric epithelial cells. Innate immune recognition of H. pylori is mediated at least in part through TLRs. In addition, H. pylori peptidoglycan (PG) can be recognized by intracellular Nod receptors (239). Interactions between H. pylori and gastric epithelial cells lead to activation of NF-κB and alteration in gene transcription in the epithelial cells. Production of IL-8 by epithelial cells leads to recruitment of neutrophils (polymorphonuclear leukocytes [PMNs]), which can phagocytose opsonized bacteria and produce reactive oxygen species (ROI) or reactive nitrogen species (RNI). The activation of mast cells results in degranulation and production of proinflammatory cytokines and chemokines.