Bacterial, environmental, population related, and individual host factors are major determinants of the outcome of Hpylori infection.^1,2 Many bacterial virulence genes—including the pathogenicity island cagA, the s1m1 vacA alleles, babA2, sabA, and oipA—have been associated with a higher degree of gastric mucosal inflammation, intestinal metaplasia, gastric or duodenal ulcer, gastric adenocarcinoma, and MALToma.^1,3–7Hpylori triggers and maintains gastric mucosal inflammation by different mechanisms, which are partly strain dependent and partly strain independent.¹ T and B lymphocyte activation and infiltration of the gastric mucosa depend on Hpylori antigen processing. The number of infiltrating polymorphonuclear cells varies depending on the virulence of the infecting strain, being much greater when infections are caused by cagA positive strains.^3,5,7–9

The inflammatory cells infiltrating Hpylori infected gastric mucosa produce a pattern of proinflammatory cytokines.^10,11 High mucosal levels of mononuclear cytokines (IL8, IL6, IL1β, tumour necrosis factor α (TNFα), and interferon γ (IFNγ)) and lymphocytic derived cytokines (IL2, IL2R) have been described in Hpylori infected patients.^10–13Hpylori infection also induces the production of IL12,^14–16 a heterodimeric proinflammatory protein that triggers the production of IFNγ and favours the differentiation of T helper 1 (Th1) cells,^17,18 which, in Hpylori infected mucosa, prevail over Th2 cells.^15,16,19 The ability of IL12 to induce Th1 is one of the biological bases of the importance of this cytokine in resisting most bacteria, including Hpylori, and also intracellular protozoa and fungal pathogens.^18,20,21 Cellular sources of IL12 in response to infections are mainly dendritic cells and phagocytes.^16–21 The two subunits of IL12—p35 and p40—are encoded by different genes, named IL12A and IL12B respectively, which are unrelated …