A mathematical model of partial-thickness burn-wound infection by Pseudomonas aeruginosa: quorum sensing and the build-up to invasion.
Pseudomonas aeruginosa remains a significant pathogen in burn-wound infection, its pathogenicity being associated with the production of a cocktail of virulence determinants which is regulated by a population-density-dependent mechanism termed quorum sensing. Quorum sensing is effected through the production and binding of signalling molecules. Here we present a mathematical model for the early stages of the infection process by P. aeruginosa in burn wounds which accounts for the quorum sensing system and for the diffusion of signalling molecules in the burn-wound environment. The results of the model and the effects of important parameters are discussed in detail. For example, the effect of the degradation rate of signalling molecules and its significance for anti-signalling therapies is discussed.
Koerber
A J
AJ
Division of Theoretical Mechanics, School of Mathematical Sciences, University of Nottingham, Nottingham NG7 2RD, U.K.
King
J R
JR
Ward
J P
JP
Williams
P
P
Croft
J M
JM
Sockett
R E
RE
D015107:4-Butyrolactone / Q000031:analogs & derivatives* / Q000502:physiology; D002056:Burns / Q000382:microbiology* / Q000473:pathology; D006714:Homoserine / Q000031:analogs & derivatives* / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D009716:Numerical Analysis, Computer-Assisted; D011552:Pseudomonas Infections / Q000382:microbiology* / Q000473:pathology; D011550:Pseudomonas aeruginosa
C109860:N-(3-oxododecanoyl)homoserine lactone; D006714:Homoserine; D015107:4-Butyrolactone