Background-It has been proposed that a pathogenic eVect of Helicobacter pylori is a weakening of the protective mucus barrier; however, this remains controversial. Aims-To clarify the eVects of H pylori infection on the mucus gel barrier in vivo.Methods-Mucus gel polymeric structure and the thickness of the adherent mucus barrier were measured in endoscopic biopsy samples in subjects with and without H pylori infection. Results-There was a significant 18% reduction in the proportion of polymeric gel forming mucin in the adherent mucus layer in H pylori positive compared with negative subjects. There was no change in the adherent mucus thickness between H pylori positive and negative subjects without gastric atrophy (mean (SD): 104 (26) µm, 106 (30) µm respectively). There was however a significant reduction in mucus thickness in those H pylori positive subjects with underlying gastric atrophy (84 (13) µm, p=0.03) compared with those without atrophy. Conclusions-A partial breakdown in gel forming structure of the gastric mucus barrier does occur in H pylori infection per se but this is insuYcient to cause a collapse of the mucus barrier. (Gut 1998;43:470-475) Keywords: Helicobacter pylori; gastric mucus Helicobacter pylori infection leads to gastritis and is an aetiological factor in the pathogenesis of peptic ulceration.1 H pylori is located within the adherent mucus barrier, particularly in the region of the gastric pit, close to the mucosal surface.2 The mucus barrier, together with epithelial bicarbonate secretion, is considered to be the first line of mucosal defence against acid and pepsin.3 This mucus layer also provides a protective environment for H pylori to colonise. 4 However, it is controversial whether or not H pylori colonisation results in changes in mucus structure and production, thereby impairing its protective eYcacy.A weakening of the mucus barrier by H pylori, leading in some cases to its collapse, has been proposed, based on the demonstration in vitro of a mucolytic proteinase in filtrates from cultures of H pylori.5 6 However, other groups have failed to show significant amounts of proteinase activity in either culture filtrates or extracts of H pylori.7-9 A non-proteolytic, urea dependent breakdown of the mucus gel by filtrates of H pylori has been observed and explained by urease activity producing ammonium ions which disrupted mucus lipid interactions.8 A study in vivo looking at mucus gel in gastric washouts, but not from the adherent mucus gel barrier, showed that mucus viscosity from H pylori infected subjects was not reduced compared with that from noninfected subjects.10 One study in vivo, observing unfixed sections of gastric mucosal biopsy specimens, showed an up to 50% reduction in mean mucus thickness of the adherent mucus gel barrier in patients with H pylori infection, compared with non-infected controls.11 Recently decreased expression of MUC5AC and aberrant expression of the glandular mucin MUC6 in gastric epithelial cells has been shown to occur with H pylori in...

Effects of HeGcobacter &on colonisation on the adherent were therefore conducted to examine the effect of NHIOH and gastric mucus barrier H.pylori urease on purified polymeric porcine gastric mucin. The intrinsic viscosity, [q] of mucin was measured after incubating LINDSEY OLIVER, JULIA L NEWON, NCOLA JORDAN, with pH 7.0 phosphate buffer, 10 mM NH40H (pH 10.2), or 59 PAUL GODDARD* PETER DEnMAR*, JEFFREY mM NH40H (pH 11.2) for 24h at 37°C. Mean [q] values (ml mg-PEARSON and ADRIAN ALLEN f SEM), determined at 25 "C in 0.2M NaCl + 0.02% NaN2, were