In situ expression of cell adhesion molecules in chronic gastritis with Helicobacter pylori infection

Helicobacter pylori infection of the stomach results in acute inflammation followed by chronic inflammation, but the mechanism is unknown. Adhesion molecules such as ICAM-1, Mac-1, and LFA-1 may help regulate interactions of immune cells and inflammatory cells. We used immunohistochemistry to locate these molecules in the gastric mucosa of patients with chronic gastritis arising from H. pylori infection. Biopsy specimens were taken from five H. pylori-negative healthy volunteers and 20 H. pylori-positive patients with chronic gastritis for immunohistochemical studies of adhesion molecules. In the gastric mucosa of patients with H. pylori-associated chronic gastritis, ICAM-1 expression was prominent in most of the vessels and inflammatory cells, such as lymphocytes and granulocytes, in the lamina propria. However, no intraepithelial lymphocytes and surface epithelial cells expressed ICAM-1. Antigen-presenting cells (APCs), such as macrophages, expressed ICAM-1 as well as HLA-DR antigen. LFA-1 and Mac-1 were strongly expressed in these immune and inflammatory cells. The number of vascular endothelial cells positive for P-selectin was also greater in H. pylori-positive mucosa. The expression of these molecules decreased remarkably after successful eradication of H. pylori. In conclusion, ICAM-1 is the predominant form among the cell adhesion molecules that are expressed in response to chronic H. pylori infection. The increased expression of ICAM-1 is linked with massive infiltration of inflammatory cells that express LFA-1 and Mac-1, and also with APCs that express HLA-DR, suggesting that ICAM-1 exerts a key role in immuno-inflammatory responses in gastric mucosa of patients with H. pylori-associated gastritis.