The pathogenic bacteria Helicobacter pylori has evolved glycan-mediated mechanisms to evade host immune recognition. For example, H. pylori incorporates Lewis blood group antigens at the terminus of liposaccharides to mimic the blood groups found on human cells, and feign self. This study tests the hypothesis that disruption of H. pylori glycan biosynthesis enhances immune recognition. To test this hypothesis, human adenocarcinoma-derived gastric epithelial cells, as well as leukemia-derived THP-1 monocytes, differentiated into dendritic cells, were challenged with wildtype H. pylori alongside an array of H. pylori glycosylation mutants, and the relative levels of immune response were measured. As a proxy for immune response, gastric epithelial cell cytokine production, dendritic cell maturation, and gastric cell granularity were measured and compared. The outcomes of this study show that H. pylori’s glycoproteins and lipopolysaccharide appear to play an important role in modulating the host immune response.

Investigating the role of Helicobacter pylori glycan biosynthesis in evading host immune cell recognition

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