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9 - Bacterial quorum sensing signalling molecules as immune modulators
- from Part III - Evasion of cellular immunity
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- By David Pritchard, Immune Modulation Research Group, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Doreen Hooi, Immune Modulation Research Group, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Eleanor Watson, Sek Chow, Immune Modulation Research Group, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Gary Telford, Immune Modulation Research Group, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Barrie Bycroft, Immune Modulation Research Group, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Siri Ram Chhabra, Department of Medicinal Chemistry, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Christopher Harty, Department of Medicinal Chemistry, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Miguel Camara, Department of Molecular Microbiology, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Stephen Diggle, Department of Molecular Microbiology, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK, Paul Williams, Department of Molecular Microbiology, School of Pharmaceutical Sciences and Institute of Infection and Immunity, University of Nottingham, Nottingham NG7 2RD, UK
- Edited by Brian Henderson, University College London, Petra C. F. Oyston, Defence Science and Technology Laboratory, Salisbury
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- Book:
- Bacterial Evasion of Host Immune Responses
- Published online:
- 13 August 2009
- Print publication:
- 28 April 2003, pp 201-222
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- Chapter
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Summary
INTRODUCTION
For many pathogens, the outcome of the interaction between host and bacterium is strongly influenced by bacterial population size. Coupling the production of virulence determinants with cell population density ensures that the host lacks sufficient time to mount an effective defence against consolidated attack. Such a strategy depends on the ability of an individual bacterial cell to sense other members of the same species and, in response, differentially express specific sets of genes. Such bacterial cell-to-cell communication or “quorum sensing” describes the phenomenon whereby the accumulation of a diffusible, low molecular weight signal molecule (sometimes referred to as a “pheromone” or “autoinducer”) enables individual bacterial cells to sense when the minimal population unit or “quorum” of bacteria has been achieved for a concerted population response to be initiated. Quorum sensing thus constitutes a mechanism for multicellular behaviour in prokaryotes and is now known to control many different aspects of bacterial physiology including the production of virulence determinants in animal, fish, and plant pathogens. A number of chemically distinct quorum sensing signal molecules (QSMs) have been described of which the N-acylhomoserine lactone (AHL) family in Gram-negative bacteria has been the most intensively investigated (for reviews see Salmond et al., 1995; Fuqua et al., 1996; Dunny and Winans, 1999; Williams et al., 2000; Withers et al., 2001). The acyl groups of the naturally occurring AHLs identified to date range from 4 to 14 carbons in length and may be saturated or unsaturated with or without a C3 substituent (usually hydroxy or oxo; see Fig. 9.1).