Helicobacter pylori and endothelial adhesion molecules: DISCUSSION (Part 3)

The cagA and vacA genes have been reported to be related to the pathogenecity of H pylori strains, especially with respect to cytokine production from epithelial cells . In the present study, though all strains had both genes, there was no relation between these genes and upregulation of adhesion molecules on HUVEC. In our fractionation study, low-molecular-weight fractions (approximately 7 kDa) showed peak adhesion molecule-inducing activity. This fraction showed a nonprotein character, resisting heat and trypsin incubation.

This substance may be the same one as inducing IL-8 production from gastric epithelial cells, as previously described. Some investigators have reported that water-soluble components derived from H pylori organisms activate leukocytes. Evans et al purified a neutrophil-activating protein (150 kDa protein), which upregulated CD11b/CD18 on neutrophils. Tufano et al have demonstrated that porins (30 kDa proteins in surface membranes) affect neutrophil chemotaxis and induce cytokine production by monocytes.

Mai et al have shown that a surface protein, urease, induces chemotactic activity in neutrophils and monocytes, and activates monocytes. Craig et al have reported a low molecular (less than 3 kDa), heat-stable, acid-resistant factor that is chemotactic for monocytes and neutrophils. In the present study, we described a low molecular (approximately 7 kDa) nonprotein substance. These results indicate that the adhesion molecule-inducing factor in HPE is neither neutrophil-activating protein, urease, nor the substance reported by Craig et al.

 

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