Abstract
Mucus is a biological gel that lines all wet epithelia in the body, including the mouth, lungs, and digestive tract, and has evolved to protect the body from pathogenic infection. However, microbial pathogenesis is often studied in mucus-free environments that lack the geometric constraints and microbial interactions in physiological three-dimensional mucus gels. We developed fluid-flow and static test systems based on purified mucin polymers, the major gel-forming constituents of the mucus barrier, to understand how the mucus barrier influences bacterial virulence, particularly the integrity of Pseudomonas aeruginosa biofilms, which can become resistant to immune clearance and antimicrobial agents. We found that mucins separate the cells in P. aeruginosa biofilms and disperse them into suspension. Other viscous polymer solutions did not match the biofilm disruption caused by mucins, suggesting that mucin-specific properties mediate the phenomenon. Cellular dispersion depended on functional flagella, indicating a role for swimming motility. Taken together, our observations support a model in which host mucins are key players in the regulation of microbial virulence. These mucins should be considered in studies of mucosal pathogenesis and during the development of novel strategies to treat biofilms.
Highlights
Despite the importance of mucins in regulating pathogens, microbial physiology in these mucosal systems is often studied in mucus-free environments, which lack the biochemistry and geometric constraints found in physiological, three-dimensional mucus gels
We report that mucin polymers induce the disassembly of P. aeruginosa biofilms
Mucin-induced biofilm dispersion depended on the flagellar cap encoded by fliD and flagellar stators encoded by motABCD, suggesting that flagellar motility is one component of the disassembly mechanism
Summary
The gel-forming biopolymers that comprise mucus, called mucins, form bottlebrush-like structures with dense O-linked glycosylation[12,13] and are important in maintaining health. Mucins regulate the motility of Helicobacter pylori[23] and suppress hyphae formation in C. albicans.[21] Despite the importance of mucins in regulating pathogens, microbial physiology in these mucosal systems is often studied in mucus-free environments, which lack the biochemistry and geometric constraints found in physiological, three-dimensional mucus gels
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