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Restricted Access Thesis

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First Advisor

Danielle Dube


Helicobacter pylori is a pathogenic bacterium that utilizes its surface glycans to modulate its interactions with host cells. H. pylori incorporates Lewis blood group tetrasaccharide antigens at the terminus of its lipopolysaccharide to mimic mammalian glycans of a host cell and glycosylates specialized proteins to facilitate its adhesion to the epithelium. This study tests the hypothesis that genetic disruption of glycan biosynthesis will negate the modulatory effects of H. pylori’s glycans and reduce the bacterium’s pathogenicity. Namely, we test the hypothesis that phase variable expression of certain carbohydrate epitopes within H. pylori’s glycocalyx accounts for variable immune response to different glycosylation mutant strains. We additionally test the hypothesis that disrupted glycan biosynthesis will inhibit effective bacterial cell adhesion. These hypotheses were tested by investigating H. pylori’s phase variable glycan architecture in parallel with the induced immune response and adhesion of different glycosylation mutant strains compared to wildtype H. pylori. Our results suggest that LPS elaboration, rather than Lewis Y antigen expression, correlates with the induced immune response of gastric epithelial cells and dendritic cells. We additionally conclude that adhesion of H. pylori to gastric epithelial cells is mediated by the glycan biosynthetic pathway.


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