Background and Aims: There is a debate whether the majority of gastritis mucosal injury occurs as a direct effect of H. pylori infection or as a result of immune cell damage from abundant mediators of inflammatory response. Recently, Urocortin (UCN) has emerged as a mediator of gastrointestinal (GI) responses to noxious stimuli. Interleukins-1β (IL-1β) and interleukin-10 (IL-10) may play important roles in gastric inflammation caused by H. pylori infection. We aimed to localize UCN 1, IL-1β, and IL-10 in gastric biopsies to elucidate their possible role in local inflammatory response before and after medical eradication of H. pylori infection. Patients and Methods: Gastric biopsies were obtained from 72 patients with dyspeptic symptoms. Specimens were examined for gastritis, presence or absence of H. pylori and immunohistochemically for UCN-1, IL-1β and IL-10 expression. Results: H. pylori was positive in 39/72 (54.2%) cases. There were significant differences in antral activity and inflammatory scores, UCN-1 and IL-1β expression between H. pylori positive and H. pylori negative patients (P<0.002, <0.03, <0.002 and <0.03 respectively). In H. pylori positive patients; eradication therapy has significantly reduced activity and chronicity of gastritis, increased UCN-1 and reduced IL-1β and IL-10 immunostaining (P<0.002, <0.002, <0.001, <0.000 and <0.000 respectively). There were significant negative, positive and no correlation between activity of gastritis and UCN-1, IL-1β (P<0.03 and <0.02) and IL-10 immunostaining respectively. Conclusion: UCN-1 may be involved in local anti-inflammatory process in active gastritis. IL-1β is considered a marker of inflammation as it increased with increasing severity of gastritis and markedly decreased after treatment.