Helicobacter pylori and endothelial adhesion molecules: DISCUSSION (Part 1)
In the present study, we demonstrated that HPE derived from NCTC11637 induces upregulation of ICAM-1, VCAM-1 and E-selectin on HUVEC. These adhesion molecules play very important roles in leukocyte-endothelial cell interactions which are the initial steps in local inflammation. Inflammatory mediators or cytokines which are increased on tissues by various stimulants activate endothelial cells, and ICAM-1, VCAM-1, E-selectin and other adhesion molecules are expressed on endothelial cells. ICAM-1 has been proposed to mediate sticking and transmigration of neutrophils. VCAM-1 can mediate rolling, sticking and transmigration of mononuclear leukocytes. E-selectin plays an important role in rolling of leukocytes. We have reported that HPE induces adhesion between neutrophils and endothelial cells via upregulation of CD11/CD18, a ligand for ICAM-1, expressed on neutrophils in vitro and in vivo. This previous study showed the importance of neutrophil activation in H pylori-induced gastric mucosal injury. However, there are only a few in vivo studies of the expression of adhesion molecules on endothelial cells in H pylori-infected gastric mucosa. Recently, it has been reported that coincubation between the H pylori organism and cultured endothelial cells results in the increased expression of endothelial adhesion molecules.