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. 2014 Aug 14;20(30):10368–10382. doi: 10.3748/wjg.v20.i30.10368

Figure 1.

Figure 1

Signal transduction and immune response in Helicobacter pylori infected gastric epithelial cells. A: VacA-induced apoptosis; B: NF-κB pathway; C: Mitogen-activated protein kinase pathway; D: Nox-1 pathway; E: IL-8/neutrophil pathway[5,8-12,14-17,19,25-39]. LPS: Lipopolysaccharide; IL: Interleukin; TLR4: Toll-like receptor 4; NF-κB: Nuclear factor-kappaB; NIK: NF-κB-inducing kinase; VacA: Vacuolating cytotoxin A; CagA: Cytotoxin-associated gene antigen; PAK1: p21-activated kinase; IKKα/β: IκB kinase α/β; MAPK: Mitogen-activated protein kinase; MKK4: MAPK kinase 4; MEK1/2: MAPK/ERK kinase 1/2; INF-γ: Interferon-γ; TNF-α: Tumor necrosis factor-α; NOD1: Nucleotide-binding oligomerisation domain protein 1; COX-2: Cyclooxygenase-2; ICAM-1: Intercellular adhesion molecule-1; iNOS: Inducible nitric oxide synthase.