In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-kappaB regulates the expression of inflammatory genes. NF-kappaB is activated by phosphorylation of its endogenous inhibitor, IkappaBalpha. The possible involvement of mitogen-activated protein kinase (MAPK) on NF-kappaB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkappaBalpha and whether H. pylori-induced phosphorylation of IkappaBalpha is mediated by MAPK in gastric epithelial AGS cells. AGS cells were treated with MAPK inhibitors (U0126 for extracellular signal-regulated kinase, SB203580 for p38 kinase, SP600125 for c-Jun NH2-terminal protein kinases) and stimulated with H. pylori. As a result, H. pylori increased phospho-specific IkappaBalpha accompanied with the decrease in control IkappaBalpha. H. pylori-induced phosphorylation of IkappaBalpha was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IkappaBalpha in H. pylori-infected AGS cells.