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Mucins trigger dispersal of Pseudomonas aeruginosa biofilms
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 micr...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6180003/ https://www.ncbi.nlm.nih.gov/pubmed/30323945 http://dx.doi.org/10.1038/s41522-018-0067-0 |
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author | Co, Julia Y. Cárcamo-Oyarce, Gerardo Billings, Nicole Wheeler, Kelsey M. Grindy, Scott C. Holten-Andersen, Niels Ribbeck, Katharina |
author_facet | Co, Julia Y. Cárcamo-Oyarce, Gerardo Billings, Nicole Wheeler, Kelsey M. Grindy, Scott C. Holten-Andersen, Niels Ribbeck, Katharina |
author_sort | Co, Julia Y. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6180003 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-61800032018-10-15 Mucins trigger dispersal of Pseudomonas aeruginosa biofilms Co, Julia Y. Cárcamo-Oyarce, Gerardo Billings, Nicole Wheeler, Kelsey M. Grindy, Scott C. Holten-Andersen, Niels Ribbeck, Katharina NPJ Biofilms Microbiomes Article 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. Nature Publishing Group UK 2018-10-10 /pmc/articles/PMC6180003/ /pubmed/30323945 http://dx.doi.org/10.1038/s41522-018-0067-0 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Co, Julia Y. Cárcamo-Oyarce, Gerardo Billings, Nicole Wheeler, Kelsey M. Grindy, Scott C. Holten-Andersen, Niels Ribbeck, Katharina Mucins trigger dispersal of Pseudomonas aeruginosa biofilms |
title | Mucins trigger dispersal of Pseudomonas aeruginosa biofilms |
title_full | Mucins trigger dispersal of Pseudomonas aeruginosa biofilms |
title_fullStr | Mucins trigger dispersal of Pseudomonas aeruginosa biofilms |
title_full_unstemmed | Mucins trigger dispersal of Pseudomonas aeruginosa biofilms |
title_short | Mucins trigger dispersal of Pseudomonas aeruginosa biofilms |
title_sort | mucins trigger dispersal of pseudomonas aeruginosa biofilms |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6180003/ https://www.ncbi.nlm.nih.gov/pubmed/30323945 http://dx.doi.org/10.1038/s41522-018-0067-0 |
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