Affiliation:
1. Molecular Microbiology and Immunology Department, Oregon Health and Sciences University, Portland, Oregon, USA
Abstract
One of the first lines of defense present at mucosal epithelial tissues is mucus, which is a highly viscous material formed by mucin glycoproteins. Mucins serve various functions, but importantly they aid in the clearance of pathogens and debris from epithelial barriers and serve as innate immune factors. In this study, we describe a requirement of host monosaccharides, likely derived from host mucins, for the ability of
Pseudomonas aeruginosa
to colonize the intestine and ultimately cause death in
Caenorhabditis elegans
. We also demonstrate that monosaccharides alter the ability of bacteria to bind to both
Caenorhabditis elegans
intestinal cells and human lung alveolar epithelial cells, suggesting that there are conserved mechanisms underlying host-pathogen interactions in a range of organisms. By gaining a better understanding of pathogen-mucin interactions, we can develop better approaches to protect against pathogen infection.
Funder
HHS | NIH | National Institute of Allergy and Infectious Diseases
HHS | NIH | National Institute of General Medical Sciences
HHS | NIH | National Heart, Lung, and Blood Institute
Publisher
American Society for Microbiology
Cited by
36 articles.
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