(316f) Invited Speaker: Role of Chemotactic Adaptation in H. Pylori Invasion and Colonization

Helicobacter pylori, a gram-negative bacterium is a leading cause of gastric cancer (non-cardia gastric cancer), and it significantly increases the risk of ulcers, gastric mucosa-associated lymphoid tissue lymphoma and gastric cancers. Typically, the lack of early symptoms delays the detection of gastric cancer till it invades muscularis propria, consistent with the poor survival rates. It is estimated that almost 60% of human beings carry these bugs, and colonization of the gastric environment typically persists throughout the life of an un-medicated host. Studies have suggested that motility and chemotaxis in H. pylori are key virulence factors, likely enabling cells to invade and subsequently colonize the stomach-epithelia. However, the genes that encode the enzymes responsible for chemotactic adaptation, which are crucial for temporal detection of chemical concentrations, are missing in H. pylori. This is at odds with recent reports that indicate that H. pylori undergo chemotaxis. I will discuss ongoing efforts in our lab to determine if chemotactic adaptation is possible in H. pylori, despite the lack of adaptation enzymes. I will present a novel approach for quantitative measurements of chemotactic activity from swimming trajectories of individual cells near surfaces. Through a combination of optical trapping that enables single motor assays, phase microscopy, and dark field-based sensitive detection of flagellar rotations, we have observed anisotropic rotation modes in flagellar bundles. We have exploited these modes to overcome current technical limitations that prevent single cell measurements. These modes appear to be arise consistently across bacterial species. We anticipate that our results will facilitate the development of antivirulence strategies to minimize the potential for invasion and colonization by H. pylori.