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Figure 2. Infection by Helicobacter pylori causes gastrin hypersecretion while reduces the secretion of somatostatin. Several mechanisms have been proposed for these hormonal changes: 1) rebound response to the elevated pH that accompanies the infection; 2) effect of the ammonia generated by bacterial urease on gastrin-secreting G cells; 3) direct effects of bacterial components on endocrine cells; 4) stimulatory effect of pro-inflammatory cytokines released from infiltrated leukocytes on G cells. Considering the proinflammatory effect of gastrin, the presence of CCK-2 receptors in polymorphonuclear leukocytes and macrophages, and the inhibitory effect of a CCK-2 receptor antagonist on the inflammation induced by H. pylori observed in the present study, we postulate that gastrin, released in response to HP-induced inflammation, aids the recruitment of leukocytes by activating local macrophages or granulocytes and contributes to the persistence of the inflammatory process. Thus, our theory is that gastrin released in response to local inflammation exerts a positive feedback on the H. pylori induced gastritis. HP, Helicobacter pylori; EpC, epithelial cells; PMN, polymorphonuclear leukocytes; MØ, macrophages; EC, endothelial cells. Continuous lines denote positive influences; dotted lines denote negative influences.
