Helicobacter pylori interacts with heparin and heparin-dependent growth factors |
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Authors: | Felipe Ascencio Hans-Arne Hansson Olle Larm Torkel Wadström |
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Institution: | Department of Marine Pathology, Center for Biological Research, La Paz, BCS 23000, México;Institute of Anatomy and Cell Biology, University of Göteborg, Medicinaregatan 5, S-413 90 Göteborg, Sweden;Department of Thoracic Surgery, Karolinska Institute, Stockholm and Medicarb AB, S-161 71 Bromma, Sweden;Department of Medical Microbiology, University of Lund, S-223 62 Lund, Sweden |
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Abstract: | Abstract The pathogenic bacterium Helicobacter pylori , which causes active, chronic type B gastritis and peptic ulcer disease, and increases the risk for development of gastric cancer, could tentatively interfere with growth factors and growth factor receptors of importance for the gastroduodenal mucosa, e.g. heparin-binding FGFs (fibroblast growth factors). H. pylori binds FGF with an extremely strong affinity (3.8 × 10−12 M), and also heparan sulfate and heparin with higher affinity ( K d 9 × 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 binding proteins (HSBP) are exposed on and shed from the surface of H. pylori , 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 resulting in disturbance of the delicate balance that control the renewal, maintenance and repair of the gastroduodenal mucosa. This mode of action has previously not been considered, but may constitute part of its pathogenic mechanism. Such a dynamic mode of action of H. pylori may explain the reason for that infected victims may either suffer from gastrointestinal symptoms or lack clinical evidence of disease or discomfort. |
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Keywords: | Helicobacter pylori Gastric ulcer Gastritis Fibroblast growth factor FGF Heparan sulfate binding proteins Heparin |
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