NFKB1 and infection: We also demonstrate that H. pylori infection of either TLR-expressing cell line induces the phosphorylation of IRAK-1 and IκB followed by NF-κB activation, which is in agreement with the hypothesis that upregulation of both TLR-2 and TLR-5 by H. pylori can switch cagPAI-dependent signalling to cagPAI-independent TLR signalling, thus may changing the outcome of infections substantially.