Differential Role of ERK and p38 on NF-κB Activation in Helicobacter pylori-Infected Gastric Epithelial Cells

Gastric cancer, as well as inflammation, caused by Helicobacter pylori, activates the production of chemokines by activation of redox-sensitive transcription factor NF- κ B in gastric epithelial cells. Mitogen-activated protein kinases including extracellular signal-regulated kinase (ERK) and p38 kinase (p38) are activated by Helicobacter pylori, which may regulate NF- κ B activation in the infected cells. However the mechanisms how ERK and p38 induce NF- κ B activation have not been investigated. Present study aims to investigate the role of ERK and p38 on the activation of NF- κ B in Helicobacter pylori-infected AGS cells. Western blot analysis was performed for determining the levels of I κ B, p105, p50 and p65 in gastric epithelial cells infected with Helicobacter pylori and treated with ERK inhibitor U0126 and p38 inhibitor SB203580. Helicobacter pylori induced the degradation of I κ Bα and upregulation of p105, p50 and p65 in the infected cells. U0126 inhibited the degradation of I κ Bα while SB203580 suppressed expression of p105, p50 and p65 in Helicobacter pylori-infected cells. ERK and p38 differentially activate NF- κ B; ERK induces degradation of I κ Bα while p38 upregulates the expression of p50 and p65, subunits of NF-κB in Helicobacter pylori-infected gastric epithelial AGS cells.