Pathogen espionage: multiple bacterial adrenergic sensors eavesdrop on host communication systems

Authors

  • Michail H. Karavolos,

    Corresponding author
    • Centre for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University, Newcastle, UK
    Search for more papers by this author
  • Klaus Winzer,

    1. School of Molecular Medical Sciences, Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
    Search for more papers by this author
  • Paul Williams,

    1. School of Molecular Medical Sciences, Centre for Biomolecular Sciences, University of Nottingham, Nottingham, UK
    Search for more papers by this author
  • C. M. Anjam Khan

    Corresponding author
    • Centre for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University, Newcastle, UK
    Search for more papers by this author

For correspondence. E-mail anjam.khan@ncl.ac.uk; Tel. (+44) 191 222 7066; Fax (+44) 191 222 7424;

E-mail michail.karavolos@ncl.ac.uk; Tel. (+44) 191 222 8147; Fax (+44) 191 222 7736.

Summary

The interactions between bacterial pathogens and their eukaryotic hosts are vital in determining the outcome of infections. Bacterial pathogens employ molecular sensors to detect and facilitate adaptation to changes in their niche. The sensing of these extracellular signals enables the pathogen to navigate within mammalian hosts. Intercellular bacterial communication is facilitated by the production and sensing of autoinducer (AI) molecules via quorum sensing. More recently, AI-3 and the host neuroendocrine (NE) hormones adrenaline and noradrenaline were reported to display cross-talk for the activation of the same signalling pathways. Remarkably, there is increasing evidence to suggest that enteric bacteria sense and respond to the host NE stress hormones adrenaline and noradrenaline to modulate virulence. These responses can be inhibited by α and β-adrenergic receptor antagonists implying a bacterial receptor-based sensing and signalling cascade. In Escherichia coli O157:H7 and Salmonella, QseC has been proposed as the adrenergic receptor. Strikingly, there is an increasing body of evidence that not all the bacterial adrenergic responses require signalling through QseC. Here we provide additional hypotheses to reconcile these observations implicating the existence of alternative adrenergic receptors including BasS, QseE and CpxA and their associated signalling cascades with major roles in interkingdom communication.

Ancillary