Your browser doesn't support javascript.
loading
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.
Afiliación
  • Co JY; 1Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
  • Cárcamo-Oyarce G; 2Microbiology Graduate Program, Massachusetts Institute of Technology, Cambridge, MA USA.
  • Billings N; 3Research Laboratory of Electronics, Massachusetts Institute of Technology, Cambridge, MA USA.
  • Wheeler KM; 1Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
  • Grindy SC; 1Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
  • Holten-Andersen N; 2Microbiology Graduate Program, Massachusetts Institute of Technology, Cambridge, MA USA.
  • Ribbeck K; 4Department of Materials Science and Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
Article en En | MEDLINE | ID: mdl-30323945
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.

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: NPJ Biofilms Microbiomes Año: 2018 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: NPJ Biofilms Microbiomes Año: 2018 Tipo del documento: Article