Helicobacter pylori infection, well known as the cause of chronic active gastritis and peptic ulcer, is associated with gastric mucosal injury. Mucosal infiltration by leukocytes is seen histologically in H pylori infection . Infiltration by leukocytes into gastric mucosa is associated with interactions between leukocytes and endothelial cells. This interaction is the initial important event in inflammation and is mediated by adhesion molecules expressed on both cell types. This interaction consists of three steps: rolling, sticking and transmigration.
Leukocyte rolling on the vascular endothelium is mediated mainly by the selectins and selectin ligands. P-selectin and E-selectin on activated endothelial cells are involved in an initial slowing of leukocytes. Leukocyte sticking and transmigration are mediated by integrins on leukocytes and immunoglobulin superfamilies on endothelial cells . Adhesion molecules in the immunoglobulin superfamily include intercellular adhesion molecule-1 (ICAM-1), platelet endothelial cell adhesion molecule-1, and vascular cell adhesion molecule-1 (VCAM-1). Although previous studies have demonstrated that leukocytes are chemoattracted by cytokines from epithelial cells or activated by H pylori proteins, only a few authors have investigated the activation of endothelial cells, the initial important event in inflammation, in H pylori-induced mucosal injury in vivo. Furthermore, there are no reports examining whether products of H pylori, but not intact living H pylori, induce upregulation of adhesion molecules on endothelial cells in vitro.