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Quorum sensing and the population dependent control of virulence.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • Paul Williams
  • Miguel Camara
  • A. Hardman
  • S. Swift
  • D. Milton
  • V. J. Hope
  • Klaus Winzer
  • B. Middleton
  • D. I. Pritchard
  • B. W. Bycroft
<mark>Journal publication date</mark>28/05/2000
<mark>Journal</mark>Philosophical Transactions of the Royal Society B: Biological Sciences
Issue number1397
Number of pages14
Pages (from-to)667-680
Publication StatusPublished
<mark>Original language</mark>English


One crucial feature of almost all bacterial infections is the need for the invading pathogen to reach a critical cell population density sufficient to overcome host defences and establish the infection. Controlling the expression of virulence determinants in concert with cell population density may therefore confer a significant survival advantage on the pathogen such that the host is overwhelmed before a defence response can be fully initiated. Many different bacterial pathogens are now known to regulate diverse physiological processes including virulence in a cell-density-dependent manner through cell-cell communication. This phenomenon, which relies on the interaction of a diffusible signal molecule (e.g. an N -acylhomoserine lactone) with a sensor or transcriptional activator to couple gene expression with cell population density, has become known as 'quorum sensing' . Although the size of the 'quorum' is likely to be highly variable and influenced by the diffusibility of the signal molecule within infected tissues, nevertheless quorum-sensing signal molecules can be detected in vivo in both experimental animal model and human infections. Furthermore, certain quorum-sensing molecules have been shown to possess pharmacological and immunomodulatory activity such that they may function as virulence determinants per se. As a consequence, quorum sensing constitutes a novel therapeutic target for the design of small molecular antagonists capable of attenuating virulence through the blockade of bacterial cell-cell communication.