Sulfated glycans on oral mucin as receptors for Helicobacter pylori

Helicobacter pylori is able to colonize gastric epithelia, causingchronic active gastritis, gastric and duodenal ulcers and presumablygastric malignancies. Attempts to identify the natural reservoirfor this microorganism other than the stomach have been unsuccessful.It is suspected that H.pylori can be transmitted orally, sincethe microorganism has been detected at various sites of theoral cavity. The aim of the present study was to determine whetherH.pylori can bind to salivary mucins, which in vivo coat theoral epithelia, and characterize further the interaction. Bindingof salivary mucins and of synthetic oligosaccharides was studiedIn ELISA and immunoblotting, using specific mono-and polyclonalantibodies, and synthetic neoglycoconjugates. H.pylori boundmost avidly to a highly sulfated sub-population of high molecularweight salivary mucins, secreted from the palatine salivaryglands, and with less avidity to mucin species secreted by thesublingual and submandibular salivary glands, which are lesssulfated. Binding was strongly enhanced upon decreasing pH from6.0 to 5.0. Using synthetic polyacrylamide coupled oligosaccharidesit was found that SO₃-3-Gal and the SO₃-3-Lewis^a blood groupantigen bound to H.pylori. In contrast, binding of sialylatedLewis^a and Lewis^b antigens was much weaker. This study indicatesthat sulfated oligosaccharides on salivary mucins may providereceptor structures for adhesion of H.pylori to oral surfaces. H.pylori saliva sulfomucin nickel oligosaccharide