The inflammatory response associated with CagA-positive H. pylori gastritis is due to the upregulated expression of proinflammatory cytokines, including tumor necrosis factor (TNF)-α, interferon gamma, interleukin- (IL-) 1beta and IL-8, and, particularly, IL-17, a key cell element in the inflammation caused by H. pylori, which mediates the activation of polymorphonuclear neutrophils [15]. Here, TNF is linked to gastritis.