The etiology of PUD is not fully understood, but it is generally accepted that it results from impaired homeostasis of gastroprotective factors, such as the mucosal-bicarbonate barrier and prostaglandin secretion, as well as aggressive factors such as gastric acid, pepsin and Helicobacter pylori (H. pylori) infection [3], and consequently an increased production of mucosal proinflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor alpha (TNFα), interleukin-17 (IL-17) and interferon gamma (IFNγ). Here, TNF is linked to Helicobacter pylori infectious disease.