HELICOBACTER-PYLORI INTERACTS WITH HEPARIN AND HEPARIN-DEPENDENT GROWTH-FACTORS

The pathogenic bacterium Helicobacter pylori, which causes active, chr onic type B gastritis and peptic ulcer disease, and increases the risk for development of gastric cancer, could tentatively interfere with g rowth factors and growth factor receptors of importance for the gastro duodenal mucosa, e.g, heparin-binding FGFs (fibroblast growth factors) . H. pylori binds FGF with an extremely strong affinity (3.8 x 10(-12) M), and also heparan sulfate and heparin with higher affinity (K-d 9 x 10(-9) M) than FGFs bind to heparin(10(-8)-10(-9) M). FGF receptors are also dependent on heparin for their activation. Heparan sulfate bi nding proteins (HSBP) are exposed on and shed from the surface of H. p ylori, which often are localised close to the epithelial stem cells in the gastroduodenal glands. H. pylori could thus efficiently interfere with growth factors and growth factor receptors, tentatively resultin g in disturbance of the delicate balance that control the renewal, mai ntenance and repair of the gastroduodenal mucosa, This mode of action has previously not been considered, but may constitute part of its pat hogenic mechanism. Such a dynamic mode of action of H. pylori may expl ain the reason for that infected victims may either suffer from gastro intestinal symptoms or lack clinical evidence of disease or discomfort .