Furthermore, our results following infection with the P12CagAKO strain, are in line with observations suggesting cagA-independent IL-8 gene transcriptional activation and secretion, following recognition of peptidoglycans, by the intracellular Nod1 receptor [29] or H. pylori lipopolysaccharide by TLRs [45], [59] or CagL binding to integrin b1 [36]. This evidence concerns the gene S100A8 and infection.