The many roads traveled by Helicobacter pylori to NFκB activation.

Many of the pathologies linked to Helicobacter pylori are caused by the ability of the bacteria to induce chronic inflammation in the stomach of the host. One of the major transcription factors that regulate inflammation is NFκB, which is constitutively activated in many cancers including some gastric cancers. H. pylori has been shown to activate NFκB using several different bacterial components and host signaling pathways in cell-type and strain-specific ways. Our recent studies demonstrate that H. pylori utilizes its virulence factor CagA to target signaling molecule TAK1 for the activation of NFκB. In this article, we will summarize our findings together with other recent progress in the H. pylori-mediated activation of NFκB and discuss the role of CagA and TAK1 in the H. pylori-mediated activation of NFκB and gastric diseases.