Although LPS is present in membranes of Gram-negative bacteria such as H pylori and is an important nonprotein proinflammatory molecule, previous studies have shown that H pylori LPS has less biological activity than E coli LPS. We did not examine H pylori LPS directly, but 0.74 EU/mL of E coli LPS did not upregulate adhesion molecules on HUVEC. In addition, final concentrations of LPS in HPE derived from NCTC11637 were less than 0.74 EU/mL, and no correlation was found between adhesion molecule-inducing activities and LPS concentrations in HPE.
Darveau et al reported that H pylori LPS did not promote the E-selectin expression on HUVEC. Taken altogether, these findings suggest that adhesion molecule-inducing substance in HPE may not be associated with LPS. Further studies are needed to identify the factor in HPE responsible for the production of endothelial adhesion molecules.
In summary, we have demonstrated that a water-soluble, low molecular, nonprotein substance in HPE induces upregula-tion of ICAM-1, VCAM-1 and E-selectin on HUVEC. These results suggest that H pylori infection may elicit endothelial-dependent interactions with leukocytes by promoting expression of endothelial adhesion molecules, and followed by gastric mucosal inflammation.