April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
Alteration of Lipopolysaccharide Biosynthesis Impacts Polysorbate 80 Mediated Biofilm Inhibition of Pseudomonas aeruginosa
Author Affiliations & Notes
  • M. E. Zegans
    Surgery (Ophthalmology) and Microbiology,
    Dartmouth Medical School, Lebanon, New Hampshire
  • J. Lam
    Molecular and Cellular Biology, University of Guelph, Guelph, Ontario, Canada
  • C. Toutain-Kidd
    Surgery (Ophthalmology),
    Dartmouth Medical School, Lebanon, New Hampshire
  • J. H. Hammond
    Microbiology and Immunology,
    Dartmouth Medical School, Lebanon, New Hampshire
  • Footnotes
    Commercial Relationships  M.E. Zegans, None; J. Lam, Medimmune Inc., C; C. Toutain-Kidd, None; J.H. Hammond, None.
  • Footnotes
    Support  NIH Grant AI068662-01A1 and P20 RR16437 (MEZ)
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3900. doi:
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    • Get Citation

      M. E. Zegans, J. Lam, C. Toutain-Kidd, J. H. Hammond; Alteration of Lipopolysaccharide Biosynthesis Impacts Polysorbate 80 Mediated Biofilm Inhibition of Pseudomonas aeruginosa. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3900.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Polysorbate 80 (PS80) is a non ionic surfactant which inhibits biofilm formation of Pseudomonas aeruginosa (PA), a leading cause of bacterial corneal infection, at concentrations as low as 0.001%. Since polysorbate 80 is well tolerated on the ocular surface in concentrations of 1% or more, this is a clinically important finding. However, some clinical strains of PA are resistant to PS80 biofilm inhibition. Understanding the basis of PS80 resistance in clinical isolates would be useful in the development of PS80 derivatives as biofilm inhibitors suitable for use on the ocular surface.

Methods: : All genetic, biochemical and microbiologic assays were performed following previously published protocols. The Pseudomonas aeruginosa _PA14 and PA01 strains are used in all experiments other than those involving clinical isolates. Ocular and non ocular clinical isolates from Dartmouth Medical School and the Campbell Laboratory, University of Pittsburgh were also tested.

Results: : Mutation of the algC gene (PA14_23810, PA3116) converts two PS80-resistant strains (lab strain PAO1 and clinical strain PA 738) which are able to form biofilms in the presence of PS80 into strains unable to form biofilms in the presence of PS80. Complementation of these mutants with algC from a plasmidreverted them to the PS80 resistant phenotype. Importantly, PAO1 and PA738 do not over produce lipase or otherwise inactivate PS80 suggesting a novel mechanism of PS80 resistance. Our studies suggests that AlgC is exerting its effect on the PA response to PS80 via its role in the biosynthesis of lipopolysaccaride (LPS) and LPS outer core in particular since mutation of rmlC also produces a similar phenotype.

Conclusions: : Our work indicates that modifications of LPS associated with the algC mutation render previously PS80 resistant strains of PA sensitive to PS80 biofilm inhibition. This is likely the result of alteration of direct interactions between PS80 with LPS, or changes access of PS80 to the PA cell membrane. A more detailed study of these interactions should lead to insights into PS80’s effects on PA biofilm biology

Keywords: pseudomonas • bacterial disease • antibiotics/antifungals/antiparasitics 

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