Loss of social behaviours in populations of Pseudomonas aeruginosa infecting lungs of patients with cystic fibrosis.
Pseudomonas aeruginosa, is an opportunistic, bacterial pathogen causing persistent and frequently fatal infections of the lung in patients with cystic fibrosis. Isolates from chronic infections differ from laboratory and environmental strains in a range of traits and this is widely interpreted as the result of adaptation to the lung environment. Typically, chronic strains carry mutations in global regulation factors that could effect reduced expression of social traits, raising the possibility that competitive dynamics between cooperative and selfish, cheating strains could also drive changes in P. aeruginosa infections. We compared the expression of cooperative traits - biofilm formation, secretion of exo-products and quorum sensing (QS) - in P. aeruginosa isolates that were estimated to have spent different lengths of time in the lung based on clinical information. All three exo-products involved in nutrient acquisition were produced in significantly smaller quantities with increased duration of infection, and patterns across four QS signal molecules were consistent with accumulation over time of mutations in lasR, which are known to disrupt the ability of cells to respond to QS signal. Pyocyanin production, and the proportion of cells in biofilm relative to motile, free-living cells in liquid culture, did not change. Overall, our results confirm that the loss of social behaviour is a consistent trend with time spent in the lung and suggest that social dynamics are potentially relevant to understanding the behaviour of P. aeruginosa in lung infections.
Department of Zoology, Oxford University, Oxford, United Kingdom.
Natalie
N
Jiricny
Department of Systems Biology, Technical University of Denmark, Lyngby, Denmark.
Søren
S
Molin
Department of Zoology, Oxford University, Oxford, United Kingdom.
Kevin
K
Foster
School of Life Sciences, Centre for Biomolecular Sciences, University Park, University of Nottingham, Nottingham, United Kingdom.
Stephen P
SP
Diggle
Department of Zoology, Oxford University, Oxford, United Kingdom.
Pauline D
PD
Scanlan
Department of Zoology, Oxford University, Oxford, United Kingdom.
Melanie
M
Ghoul
Institute for International Health, Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Helle Krogh
HK
Johansen
Department of Zoology, Oxford University, Oxford, United Kingdom.
Lorenzo A
LA
Santorelli
Centre for Immunity, Infection and Evolution, University of Edinburgh Ashworth Labs, King's Buildings, West Mains Road, Edinburgh, United Kingdom.
Roman
R
Popat
Department of Zoology, Oxford University, Oxford, United Kingdom.
Stuart A
SA
West
Department of Zoology, Oxford University, Oxford, United Kingdom.
Ashleigh S
AS
Griffin
D018441:Biofilms / Q000254:growth & development; D002450:Cell Communication; D003550:Cystic Fibrosis / Q000382:microbiology*; D005110:Extracellular Space / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000382:microbiology*; D009842:Oligopeptides / Q000378:metabolism; D010196:Pancreatic Elastase / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D011550:Pseudomonas aeruginosa / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D017262:Siderophores / Q000378:metabolism
D009842:Oligopeptides; D017262:Siderophores; C042453:pyoverdin; D010447:Peptide Hydrolases; D010196:Pancreatic Elastase