MUCUS AND HELICOBACTER-PYLORI

A continuous, adherent mucus gel layer with mucosal bicarbonate secret ion is the initial protective barrier in the stomach and duodenum agai nst erosion by the gastric juice. H. pylori resides within the adheren t mucus gel layer close to the epithelial surface. The barrier functio n of the mucus layer in vivo depends on (i) its thickness, and (ii) it s gel structure, a property which is linearly dependent on the polymer ic mucin content. We have shown in vivo that H, pylori colonisation al one did not decrease the thickness of the adherent gastric mucus barri er, although there was a mean 20% decrease in mucus thickness in those H. pylori positive subjects with underlying gastric atrophy. There wa s, however, a significant mean 18% reduction in the gel-forming polyme ric mucin content of mucus from H. pylori subjects, independent of und erlying atrophy. Studies in vivo suggest this loss of gel structure mi ght arise from a H. pylori mediated, high local pH generated by urease activity rather than by proteolysis. This study shows that H. pylori infection alone does not compromise the overall integrity of the mucus barrier in vivo. However, in the immediate environment of the organis m there appears to be a localised loss of mucus gel structure. The muc us barrier is compromised if H. pylori associated gastric atrophy or p eptic ulceration follows.