Old and New Aspects of -Associated Inflammation and Gastric Cancer.

is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host's stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within --infected mucosa, more recent studies failed in encountering any association between IL-8 and infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an anti-inflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to --induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. uses the immunosuppressive role of IL-10 to favor its escape from the host's immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of to the host's cells and their subsequent colonization. The role of --induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with --associated gastric cancer.