Quorum sensing and signal interference: diverse implications

Abstract

SummaryQuorum sensing (QS) is a community genetic regulation mechanism that controls microbiological functions of medical, agricultural and industrial importance. Discovery of microbial QS signals and the signalling mechanisms led to identification of numerous enzymatic and non-enzymatic signal interference mechanisms that quench microbial QS signalling. Evidence is accumulating that such signal interference mechanisms can be developed as promising approaches to control microbial infection and biofilm formation. In addition, these mechanisms exist not only in microorganisms but also in the host organisms of bacterial pathogens, highlighting their potential implications in microbial ecology and in host-pathogen interactions. Investigation of QS and signal interference mechanisms might significantly broaden the scope of research in microbiology.

The rhizosphere: a playground and battlefield for soilborne pathogens and beneficial microorganisms

“…For many antagonistic bacteria living in the rhizosphere, expression of a range of genes is regulated by autoinducers, such as N-acylhomoserine lactones (AHLs), which act as intercellular signals (reviewed in Somers et al 2004;Zhang and Dong 2004). This phenomenon of cell to cell communication, also referred to as quorum sensing, drives the expression of several beneficial traits in rhizosphere bacteria and of a range of virulence traits in human and plant pathogenic bacteria (Pierson et al 1998;Zhang and Dong 2004).…”

“…This phenomenon of cell to cell communication, also referred to as quorum sensing, drives the expression of several beneficial traits in rhizosphere bacteria and of a range of virulence traits in human and plant pathogenic bacteria (Pierson et al 1998;Zhang and Dong 2004). The ability of antagonists to interfere with quorum sensing in plant pathogens provides a means to control plant diseases and to promote plant health.…”

“…Conversely, soilborne plant pathogens can utilize similar strategies to interfere with quorum-regulated antibiotic biosynthesis as a defense strategy against microbial antagonism. Several strategies of quorum sensing inhibition, also refered to as quorum quenching, have been unraveled in the past decade and include repression or blockage of the production of signal molecules, inactivation of the signal molecules or interference with signal perception (reviewed in Zhang and Dong 2004;Rasmussen and Givskov 2006). To date, two types of enzymes that inactivate AHLs have been identified in a range of bacterial species and genera; these include the AHL-lactonases that hydrolyse the lactone ring to yield acyl homoserines with reduced biological activity, and the AHL-acylases that break the amide linkage of AHLs resulting in homoserine lactone and fatty acids, which do not exhibit biological activity (reviewed in Zhang and Dong 2004;Uroz et al 2007).…”

Quorum quenching enzyme activity is widely conserved in the sera of mammalian species

“…For example, AiiA, an AHL-lactonase enzyme coded by the aiiA gene from Bacillus sp., can hydrolyze the lactone ring of AHL signals [10]. Evidence suggests that Bacillus may adopt this ability to boost its competitive strength in ecosystems [11], as some bacterial species use AHL signals to coordinate antibiotic production and the signals could spontaneously convert to bactericidal compounds [12,13]. Intriguingly, AHL inactivation activity has also been found recently in human epithelia cells and plant seedlings [14,15], implying that QS interference may also be one of innate defense mechanisms of higher organisms against microbial infections.…”

Structural basis for antiactivation in bacterial quorum sensing

“…There has been intense interest in studying the molecular mechanisms of quorum sensing to develop strategies by which to control microbial activity. Inhibition of AHL quorum sensing through chemically synthesized AHL analogs, inhibitory natural products, and AHL-degrading enzymes has achieved variable degrees of effectiveness (3). Inhibition mechanisms, however, are still required and offer the promise of ameliorating infectious disease through modulation of intercellular communication.…”