Studies on Helicobacter Pylori motility: influence of cell morphology, medium rheology, and swimming mechanism
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In this thesis, I present a detailed analysis of the role cell morphology, solution rheology, and swimming mechanism has on the motility of Helicobacter Pylori. H. Pylori, the bacterium that causes gastric ulcers, has a helical cell shape that has long been believed to provide an advantage in penetrating the viscous mucus layer protecting the stomach lining, its niche environment. I present results obtained by performing optical microscopic live cell bacteria tracking of wild-type H. Pylori and cell shape and flagella mutants of H. Pylori. Bacteria tracking experiments show that helical shaped bacteria swim faster than straight rod-shaped bacteria, and bacteria with larger number of flagella swim faster. Altering cell shape is found to have a smaller effect on swimming speed than altering the number of flagella a bacterium has. These experimental observations are then compared to resistive force theory predictions. Resistive force theory shows qualitative agreement to our experimental observations, but overestimates the increase in swimming speed for a helical cell when compared to straight rod cell. In addition to effect of cell morphology on motility, I explore how motility is altered in different polymer environments by tracking bacteria in pig gastric mucin, methylcellulose, and gelatin solutions and gels. Bacteria are found to increase their swimming speed non-monotonically with increasing polymer concentration, while the number of mobile bacteria is found to decrease with increased polymer concentration. I also present an analysis of the swimming mechanism used by H. Pylori. H. Pylori is found to use a run-reverse swimming mechanism which I model as a random walk. This random walk model fits well to the experimental data and provides a theoretical tool for interpreting H. Pylori’s swimming mechanism. Taken together these results provide a detailed description of the motility of H. Pylori in different media and are applicable to the broad question of how H. pylori infects and colonizes the mucus layer of the stomach.