Microvascular Pathophysiology in Gastric Mucosal Inflammation Associated with Helicobacter pylori Infection

Abstract

In the multitude of mechanisms involved in the development of gastricmucosal inflammation, derangement of the micro circulatory system is acommon initial pathway. In response to gastric luminal antigens such asbacteria and food factors, the microvascular endothelium transducessignals to circulating cells. Helicobacter pylori colonization induces asignificant level of leukocyte recruitment to the gastric mucosa as aresult of the sequential pathological processes in the microcirculatorysystem. This bacterial infection is associated with a variety ofclinical outcomes, including benign and malignant gastroduodenaldiseases. After H. pylori inoculation, the bacteria colonize the surfaceepithelium, upon which numerous leukocytes rolling, or adhering to theendothelial cells can be observed in the venules of the gastric mucosa.The adherent leukocytes migrate into the gastric mucosal parenchyma.Among the numerous proinflammatory factors, such as cytokines, freeradicals, and enzymes, a monochloramine, derived from both leukocytesand H. pylori, is an important factor involved in the development of H.pylori-associated disease. Persistent H. pylori infection has recentlybeen achieved in Mongolian gerbil models, in which the sequentialmicrocirculatory and histopathological changes in the gastric mucosahave been shown to closely mimic the changes leading to gastric mucosallesion formation in association with H. pylori infection in humans.Gastric mucosa infected with H. pylori exhibited significantly highergastritis scores. Because the recently isolated growth-hormone-releasingpeptide ghrelin is secreted mainly from the A-like cells in the gastriccorpus, the anatomical extension of H. pylori-associated inflammation tothe gastric corpus mucosa might also affect ghrelin secretion and itsassociated appetite control.