S100A8 and duodenal ulcer: Both CagA and the secretory system, by independent mechanisms, activate proinflammatory signals and interleukin-8 secretion.[24, 25] Furthermore, the CagA PAI-positive strains are known to induce the expression of a DNA-editing enzyme, which leads to accumulation of mutations in the tumor suppressor p53.[26] On the other hand, it had been shown that there are many CagA PAI-negative strains in gastroduodenal ulcers and gastric carcinomas.[14] Therefore, it is possible that other factors such as host immune mechanisms and environmental factors also play a role in the pathogenesis of the H.