Roger worked on how H. pylori affects epithelial cell polarity and the apical-junctional complex.
Fabio investigated how the H. pylori virulence factor CagA perturbs epithelial cell differentiation and polarity.
Mickey studied how the bacterium Listeria monocytogenes invades the intestinal epithelium. He discovered that Listeria utilize breaches in cell polarity to access its receptor E-cadherin for invasion.
Shumin elucidated how H. pylori utilizes the cell surface as a replicative niche, and how H. pylori's virulence factors CagA and VacA directly benefit the bacterium by usurping host cell polarity and iron trafficking to enable colonization.
Mike worked on chemotaxis regulatory mechanisms uniquely present in H. pylori and other Epsilonproteobacteria, and the role of chemotaxis in H. pylori colonization of the gastric glands.
Josephine developed a mouse model of H. pylori infection to look at the effects of the bacterial virulence factor CagA in vivo. Using this model, she also characterized host and bacterial factors that determine H. pylori localization in the stomach.
Julie studied the mechanisms that H. pylori uses to sense key signals in the stomach to find a specialized niche in the gastric epithelium where it can survive.
Lauren investigated how components of the host cellular adherens junctions control susceptibility to the Staphylococcus aureus virulence factor, α-toxin.
Michael used a mouse model of H. pylori infection to discover that bacteria can colonize and activate gastric epithelial stem cells.
Ryan studied H. pylori's response to epithelial cell adherence, and was developing a primary murine organoid gastric cancer model to study H. pylori infection.
Diane used electron microscopy to visualize the interface of H. pylori's Type IV secretion system with the host cell surface.
Elizabeth explored whether Yersinia enterocolitica has a similar mode of invasion of the intestinal epithelium as what we have previously shown for Listeria monocytogenes.
Lee investigated how the intestinal pathogen Yersinia enterocolitica is able to access its host receptor B1 integrin when it is normally not exposed to the apical surface in polarized epithelia.
Renee assisted Josephine Lee in characterizing a mouse model of H. pylori infection.