Helicobacter pylori induces IkappaB kinase alpha nuclear translocation and chemokine production in gastric epithelial cells.

ABSTRACT: NF-kappaB is an important transcriptional factor that is involved in multiple cellular responses, such as inflammation and antiapoptosis. IkappaB kinase alpha (IKKalpha) and IKKbeta, which are critical regulators of NF-kappaB activity, possess various mechanisms for NF-kappaB activation. This variability in NF-kappaB signaling may be associated with distinct inflammatory responses in specific cell types. The gastric pathogen Helicobacter pylori is known to activate NF-kappaB. However, the role of IKK in H. pylori infection remains unclear. In this report, we show that H. pylori activates both IKKalpha and IKKbeta in gastric cancer cells and enhances NF-kappaB signaling in distinct manners. We found that IKKbeta acted as an IkappaBalpha kinase during H. pylori infection, whereas IKKalpha di

SUBMITTER: Hirata Y 

PROVIDER: S-EPMC1418661 | biostudies-literature | 2006 Mar

REPOSITORIES: biostudies-literature