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Respiratory mucus is a viscoelastic hydrogel that serves as the first line of defense for the lungs. As we breathe, we inhale bacterial, viral, and environmental particulates into our lungs. Mucus entraps these particulates and is transported out of the lungs through coordinated ciliary beating of the bronchial epithelia, reminiscent of transporting people using an escalator, via the mechanism mucociliary clearance. The efficiency of mucociliary clearance becomes impaired when mucus concentration is altered. For instance, the concentration of airway mucus becomes abnormally high for patients with mucus-obstructive lung diseases like cystic fibrosis or chronic obstructive pulmonary disease, and the lungs become highly susceptible to bacterial infections. Although restoring the properties of mucus is critical to treatment of these diseases, this requires elucidating the roles of mucus as a physical hydrogel in defense.

In this work, I seek to develop a fuller understanding of the roles of native mucus in the context of mucociliary clearance. I focus on two aspects: (1) mucus-bacteria interactions and (2) mucus properties essential to efficient mucus clearance. I develop a method for harvesting native mucus with concentrations matching healthy and diseased airway mucus using well-differentiated human bronchia epithelial cell cultures. I quantify the transport of opportunistic pathogen Pseudomonas aeruginosa strain PA14, a human clinical isolate responsible for chronic lung infections, in this native mucus to elucidate the effects of mucus-bacteria interactions on bacteria motility. I find that PA exhibits a bimodal motility; in healthy mucus, motion is primarily linear, with a small proportion adopting a confined motion. As mucus concentration increases, PA14 exhibit an increasing propensity for confinement. With this work, I seek to unravel long-standing questions of human lung defense by understanding the mechanisms of bacterial transport through native mucus.