Bacteriocin-mediated competition in cystic fibrosis lung infections

Melanie Ghoul, Stuart A. West, Helle Krogh Johansen, Søren Molin, Odile B. Harrison, Martin C. J. Maiden, Lars Jelsbak, John B. Bruce, Ashleigh S. Griffin

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Abstract

Bacteriocins are toxins produced by bacteria to kill competitors of the same species. Theory and laboratory experiments suggest that bacteriocin production and immunity play a key role in the competitive dynamics of bacterial strains. The extent to which this is the case in natural populations, especially human pathogens, remains to be tested. We examined the role of bacteriocins in competition using Pseudomonas aeruginosa strains infecting lungs of humans with cystic fibrosis (CF). We assessed the ability of different strains to kill each other using phenotypic assays, and sequenced their genomes to determine what bacteriocins (pyocins) they carry. We found that (i) isolates from later infection stages inhibited earlier infecting strains less, but were more inhibited by pyocins produced by earlier infecting strains and carried fewer pyocin types; (ii) this difference between early and late infections appears to be caused by a difference in pyocin diversity between competing genotypes and not by loss of pyocin genes within a lineage over time; (iii) pyocin inhibition does not explain why certain strains outcompete others within lung infections; (iv) strains frequently carry the pyocin-killing gene, but not the immunity gene, suggesting resistance occurs via other unknown mechanisms. Our results show that, in contrast to patterns observed in experimental studies, pyocin production does not appear to have a major influence on strain competition during CF lung infections.
Original languageEnglish
Article number20150972
JournalProceedings of the Royal Society B: Biological Sciences
Volume282
Issue number1814
Number of pages8
ISSN0962-8452
DOIs
Publication statusPublished - 2015

Bibliographical note

Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

Keywords

  • Bacteriocins
  • Pyocins
  • Competition
  • Cystic fibrosis
  • Pseudomonas aeruginosa

Cite this

Ghoul, Melanie ; West, Stuart A. ; Johansen, Helle Krogh ; Molin, Søren ; Harrison, Odile B. ; Maiden, Martin C. J. ; Jelsbak, Lars ; Bruce, John B. ; Griffin, Ashleigh S. / Bacteriocin-mediated competition in cystic fibrosis lung infections. In: Proceedings of the Royal Society B: Biological Sciences. 2015 ; Vol. 282, No. 1814.
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Bacteriocin-mediated competition in cystic fibrosis lung infections. / Ghoul, Melanie; West, Stuart A.; Johansen, Helle Krogh; Molin, Søren; Harrison, Odile B.; Maiden, Martin C. J.; Jelsbak, Lars; Bruce, John B.; Griffin, Ashleigh S.

In: Proceedings of the Royal Society B: Biological Sciences, Vol. 282, No. 1814, 20150972, 2015.

Research output: Contribution to journalJournal articleResearchpeer-review

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AU - Ghoul, Melanie

AU - West, Stuart A.

AU - Johansen, Helle Krogh

AU - Molin, Søren

AU - Harrison, Odile B.

AU - Maiden, Martin C. J.

AU - Jelsbak, Lars

AU - Bruce, John B.

AU - Griffin, Ashleigh S.

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AB - Bacteriocins are toxins produced by bacteria to kill competitors of the same species. Theory and laboratory experiments suggest that bacteriocin production and immunity play a key role in the competitive dynamics of bacterial strains. The extent to which this is the case in natural populations, especially human pathogens, remains to be tested. We examined the role of bacteriocins in competition using Pseudomonas aeruginosa strains infecting lungs of humans with cystic fibrosis (CF). We assessed the ability of different strains to kill each other using phenotypic assays, and sequenced their genomes to determine what bacteriocins (pyocins) they carry. We found that (i) isolates from later infection stages inhibited earlier infecting strains less, but were more inhibited by pyocins produced by earlier infecting strains and carried fewer pyocin types; (ii) this difference between early and late infections appears to be caused by a difference in pyocin diversity between competing genotypes and not by loss of pyocin genes within a lineage over time; (iii) pyocin inhibition does not explain why certain strains outcompete others within lung infections; (iv) strains frequently carry the pyocin-killing gene, but not the immunity gene, suggesting resistance occurs via other unknown mechanisms. Our results show that, in contrast to patterns observed in experimental studies, pyocin production does not appear to have a major influence on strain competition during CF lung infections.

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