However, in the present study, because there is little opportunity for direct contact between bacteria and endothelial cells in gastric mucosa, we used HPE which contains water-soluble components of the membrane or the cytosol. A recent report showed that H pylori alters the barrier properties of the epithelium in vitro. Therefore, HPE, especially low molecular substance in HPE, may permeate into the gastric mucosa and directly affect the endothelial cells.
Our study is the first observation that products of H pylori, but not intact living bacteria, upregulates ICAM-1, VCAM-1 and E-selectin on endothelial cells. This suggests the following mechanism of H pylori-induced gastric mucosal injury: endothelial cells are activated by water-soluble substances released or secreted from the organism, ICAM-1, VCAM-1 and E-selectin are upregulated, and subsequently, leukocytes adhere to endothelial cells via increased adhesion molecules. Leukocytes adhering to endothelial cells emigrate into the interstitium by IL-8 released from gastric epithelial cells. Reactive oxygen species or proteases derived from leukocytes are implicated in the gastric mucosal injury associated with H pylori.