ABSTRACT
Esophagogastrointestinal inflammation is a highly complex biochemical protective response to cellular or tissue injury. When this process occurs in an uncontrolled manner, the result is excessive cellular or tissue damage, which results in chronic inflammation and destruction of normal tissue. Current evidence suggests that Helicobacter pylori infection and nonsteroidal antiinflammatory drug (NSAID) ingestion are major causative factors in the pathogenesis of gastric mucosal injury in humans, and chemical agents such as gastric acid, bile acids, and pancreatic protease also cause esophageal inflammation. However, the cause of inflammatory bowel disease is unknown. In response to H. pylori infection, NSAID, or chemical agents, neutrophils are recruited to the site of inflammation and generate reactive oxygen and nitrogen species and proteases. Extravascularly migrated neutrophils infiltrate the region around bacteria and target cells, depending on the concentration of the chemoattractants, including interleukin (IL)-8, and take actions advantageous to the body, such as killing bacteria and cancer cells; they may also injure normal cells and tissue. It has been shown that the interaction between leukocytes and vascular endothelial cells is regulated by various cell adhesion molecules and that this interaction is directly or indirectly modified by many factors including inflammatory chemokines and reactive oxygen species (ROS). In addition to
oxidative stress induced by ROS, our recent findings indicate that gas-like mediators play a crucial role in the regulation of gastrointestinal inflammation. The inhibition of inducible nitric oxide synthase attenuates esophagogastrointestinal inflammation. This paper describes the potential role of chemokine and activated neutrophils in esophagogastrointestinal inflammation induced by chemical agents, H. pylori, NSAID, and inflammatory bowel disease.
