Since the increased expression of inflammatory mediators such as COX-2, IL-1β, IL-6, IFN-γ, and IL-8 were one of core pathogenic mechanisms in H. pylori-associated gastritis [24, 25] and these inflammatory responses are thought to be one of the core processes involved in gastric carcinogenesis [26, 27], we have focused on to the serial changes of COX-2-Prostaglandin E2 (PGE2) pathway [28]. Here, CXCL8 is linked to gastritis.