Helicobacter pylori (Hp) is a Gram-negative bacteria that colonizes the stomach of over half of the global population and can lead to the development of gastric and duodenal ulcers, gastritis, and gastric cancer in the infected individuals. Successful colonization of the host stomach requires intimate interaction of Hp with the host epithelium. Although Hp’s ability to adhere to the gastric tract is glycosylation-dependent and crucial for colonization, not all of the mechanisms by which Hp interacts with host cells are well understood. Evidence from our lab and others indicates that Hp synthesizes a vast array of glycoproteins, some of which are present on the cell surface. The role of these glycoproteins in mediating host-pathogen interactions is intriguing, because surface glycoproteins mediate host-pathogen interactions in a number of bacterial pathogens. Here, we employed metabolic oligosaccharide engineering to monitor Hp’s glycoprotein expression pattern in the presence and absence of mammalian cells, with the hopes of identifying Hp glycoproteins that are crucial for host-pathogen interactions. Our results indicate that certain Hp glycoproteins are selectively over-expressed when Hp is grown in the presence of host cells rather than in monoculture. Experiments are currently underway to isolate and identify the glycoproteins that are upregulated in the presence of host cells.

Analysis of glycoproteins in Helicobacter pylori overexpressed in the presence of host cells

251st National Meeting (2016)

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