Diffusion retardation by binding of tobramycin in an alginate biofilm model

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Diffusion retardation by binding of tobramycin in an alginate biofilm model. / Cao, Bao; Christophersen, Lars; Kolpen, Mette; Jensen, Peter Østrup; Sneppen, Kim; Høiby, Niels; Moser, Claus; Sams, Thomas.

In: P L o S One, Vol. 11, No. 4, e0153616, 21.04.2016.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Cao, B, Christophersen, L, Kolpen, M, Jensen, PØ, Sneppen, K, Høiby, N, Moser, C & Sams, T 2016, 'Diffusion retardation by binding of tobramycin in an alginate biofilm model', P L o S One, vol. 11, no. 4, e0153616. https://doi.org/10.1371/journal.pone.0153616

APA

Cao, B., Christophersen, L., Kolpen, M., Jensen, P. Ø., Sneppen, K., Høiby, N., Moser, C., & Sams, T. (2016). Diffusion retardation by binding of tobramycin in an alginate biofilm model. P L o S One, 11(4), [e0153616]. https://doi.org/10.1371/journal.pone.0153616

Vancouver

Cao B, Christophersen L, Kolpen M, Jensen PØ, Sneppen K, Høiby N et al. Diffusion retardation by binding of tobramycin in an alginate biofilm model. P L o S One. 2016 Apr 21;11(4). e0153616. https://doi.org/10.1371/journal.pone.0153616

Author

Cao, Bao ; Christophersen, Lars ; Kolpen, Mette ; Jensen, Peter Østrup ; Sneppen, Kim ; Høiby, Niels ; Moser, Claus ; Sams, Thomas. / Diffusion retardation by binding of tobramycin in an alginate biofilm model. In: P L o S One. 2016 ; Vol. 11, No. 4.

Bibtex

@article{4f2f55d35bb74aef89bdbf755967da69,
title = "Diffusion retardation by binding of tobramycin in an alginate biofilm model",
abstract = "Microbial cells embedded in a self-produced extracellular biofilm matrix cause chronic infections, e. g. by Pseudomonas aeruginosa in the lungs of cystic fibrosis patients. The antibiotic killing of bacteria in biofilms is generally known to be reduced by 100-1000 times relative to planktonic bacteria. This makes such infections difficult to treat. We have therefore proposed that biofilms can be regarded as an independent compartment with distinct pharmacokinetics. To elucidate this pharmacokinetics we have measured the penetration of the tobramycin into seaweed alginate beads which serve as a model of the extracellular polysaccharide matrix in P. aeruginosa biofilm. We find that, rather than a normal first order saturation curve, the concentration of tobramycin in the alginate beads follows a power-law as a function of the external concentration. Further, the tobramycin is observed to be uniformly distributed throughout the volume of the alginate bead. The power-law appears to be a consequence of binding to a multitude of different binding sites. In a diffusion model these results are shown to produce pronounced retardation of the penetration of tobramycin into the biofilm. This filtering of the free tobramycin concentration inside biofilm beads is expected to aid in augmenting the survival probability of bacteria residing in the biofilm.",
author = "Bao Cao and Lars Christophersen and Mette Kolpen and Jensen, {Peter {\O}strup} and Kim Sneppen and Niels H{\o}iby and Claus Moser and Thomas Sams",
year = "2016",
month = apr,
day = "21",
doi = "10.1371/journal.pone.0153616",
language = "English",
volume = "11",
journal = "P L o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "4",

}

RIS

TY - JOUR

T1 - Diffusion retardation by binding of tobramycin in an alginate biofilm model

AU - Cao, Bao

AU - Christophersen, Lars

AU - Kolpen, Mette

AU - Jensen, Peter Østrup

AU - Sneppen, Kim

AU - Høiby, Niels

AU - Moser, Claus

AU - Sams, Thomas

PY - 2016/4/21

Y1 - 2016/4/21

N2 - Microbial cells embedded in a self-produced extracellular biofilm matrix cause chronic infections, e. g. by Pseudomonas aeruginosa in the lungs of cystic fibrosis patients. The antibiotic killing of bacteria in biofilms is generally known to be reduced by 100-1000 times relative to planktonic bacteria. This makes such infections difficult to treat. We have therefore proposed that biofilms can be regarded as an independent compartment with distinct pharmacokinetics. To elucidate this pharmacokinetics we have measured the penetration of the tobramycin into seaweed alginate beads which serve as a model of the extracellular polysaccharide matrix in P. aeruginosa biofilm. We find that, rather than a normal first order saturation curve, the concentration of tobramycin in the alginate beads follows a power-law as a function of the external concentration. Further, the tobramycin is observed to be uniformly distributed throughout the volume of the alginate bead. The power-law appears to be a consequence of binding to a multitude of different binding sites. In a diffusion model these results are shown to produce pronounced retardation of the penetration of tobramycin into the biofilm. This filtering of the free tobramycin concentration inside biofilm beads is expected to aid in augmenting the survival probability of bacteria residing in the biofilm.

AB - Microbial cells embedded in a self-produced extracellular biofilm matrix cause chronic infections, e. g. by Pseudomonas aeruginosa in the lungs of cystic fibrosis patients. The antibiotic killing of bacteria in biofilms is generally known to be reduced by 100-1000 times relative to planktonic bacteria. This makes such infections difficult to treat. We have therefore proposed that biofilms can be regarded as an independent compartment with distinct pharmacokinetics. To elucidate this pharmacokinetics we have measured the penetration of the tobramycin into seaweed alginate beads which serve as a model of the extracellular polysaccharide matrix in P. aeruginosa biofilm. We find that, rather than a normal first order saturation curve, the concentration of tobramycin in the alginate beads follows a power-law as a function of the external concentration. Further, the tobramycin is observed to be uniformly distributed throughout the volume of the alginate bead. The power-law appears to be a consequence of binding to a multitude of different binding sites. In a diffusion model these results are shown to produce pronounced retardation of the penetration of tobramycin into the biofilm. This filtering of the free tobramycin concentration inside biofilm beads is expected to aid in augmenting the survival probability of bacteria residing in the biofilm.

U2 - 10.1371/journal.pone.0153616

DO - 10.1371/journal.pone.0153616

M3 - Journal article

C2 - 27100887

AN - SCOPUS:84964688013

VL - 11

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 4

M1 - e0153616

ER -

ID: 168885979