Quorum Sensing and the Social Evolution of Bacterial Virulence

The ability of pathogenic bacteria to exploit their hosts depends upon various virulence factors, released in response to the concentration of small autoinducer molecules that are also released by the bacteria [1–5]. In vitro experiments suggest that autoinducer molecules are signals used to coordin...

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Bibliographic Details
Published in:Current biology 2009-02, Vol.19 (4), p.341-345
Main Authors: Rumbaugh, Kendra P., Diggle, Stephen P., Watters, Chase M., Ross-Gillespie, Adin, Griffin, Ashleigh S., West, Stuart A.
Format: Article
Language:English
Subjects:
Animal models
Animals
Bacteria
CheA protein
EVO_ECOL
Evolution
Female
Fitness
Humans
Liver - microbiology
Mice
Mixed infection
Pseudomonas aeruginosa
Pseudomonas aeruginosa - pathogenicity
Pseudomonas aeruginosa - physiology
quorum sensing
Quorum Sensing - physiology
Skin - microbiology
virulence factors
Wounds and Injuries - microbiology
Wounds and Injuries - pathology
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Summary:The ability of pathogenic bacteria to exploit their hosts depends upon various virulence factors, released in response to the concentration of small autoinducer molecules that are also released by the bacteria [1–5]. In vitro experiments suggest that autoinducer molecules are signals used to coordinate cooperative behaviors and that this process of quorum sensing (QS) can be exploited by individual cells that avoid the cost of either producing or responding to signal [6, 7]. However, whether QS is an exploitable social trait in vivo, and the implications for the evolution of virulence [5, 8–10], remains untested. We show that in mixed infections of the bacterium Pseudomonas aeruginosa, containing quorum-sensing bacteria and mutants that do not respond to signal, virulence in an animal (mouse) model is reduced relative to that of an infection containing no mutants. We show that this is because mutants act as cheats, exploiting the cooperative production of signal and virulence factors by others, and hence increase in frequency. This supports the idea that the invasion of QS mutants in infections of humans [11–13] is due to their social fitness consequences [6, 7, 14] and predicts that increased strain diversity will select for lower virulence.
ISSN:0960-9822
1879-0445
DOI:10.1016/j.cub.2009.01.050