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Glycobiology, 2000, Vol. 10, No. 11 1171-1181
© 2000 Oxford University Press

Inhibition of nonopsonic Helicobacter pylori–induced activation of human neutrophils by sialylated oligosaccharides

Susann Teneberg1, Margaretha Jurstrand2, Karl-Anders Karlsson and Dan Danielsson2

Institute of Medical Biochemistry, Göteborg University, P.O. Box 440, SE 405 30 Göteborg, Sweden, and 2Department of Clinical Microbiology and Immunology, Örebro Medical Centre Hospital, SE 701 85 Örebro, Sweden

Certain strains of Helicobacter pylori have nonopsonic neutrophil-activating capacity. Some H.pylori strains and the neutrophil-activating protein of H.pylori (HPNAP) bind selectively to gangliosides of human neutrophils. To determine if there is a relationship between the neutrophil-activating capacity and the ganglioside-binding ability, a number of H.pylori strains, and HPNAP, were incubated with oligosaccharides, and the effects on the oxidative burst of subsequently challenged neutrophils was measured by chemiluminescence and flow cytometry. Both by chemiluminescence and flow cytometry a reduced response was obtained by incubation of H.pylori with sialic acid–terminated oligosaccharides, whereas lactose had no effect. The reductions obtained with different sialylated oligosaccharides varied to some extent between the H.pylori strains, but in general 3'-sialyllactosamine was the most efficient inhibitor. Challenge of neutrophils with HPNAP gave no response in the chemiluminescence assay, and a delayed moderate response with flow cytometry. Preincubation of the protein with 3'-sialyllactosamine gave a slight reduction of the response, while 3'-sialyllactose had no effect. The current results suggest that the nonopsonic H.pylori–induced activation of neutrophils occurs by lectinophagocytosis, the recognition of sialylated glycoconjugates on the neutrophil cell surface by a bacterial adhesin leads to phagocytosis and an oxidative burst with the production of reactive oxygen metabolites.

1 To whom correspondence should be addressed


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