Quorum sensing dependent phenotypes and their molecular mechanisms in Campylobacterales.

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Quorum sensing comprises the mechanism of communication between numerous bacteria via small signalling molecules, termed autoinducers (AI). Using quorum sensing, bacteria can regulate the expression of multiple genes involved in virulence, toxin production, motility, chemotaxis and biofilm formation, thus contributing to adaptation as well as colonisation. The current understanding of the role of quorum sensing in the lifecycle of Campylobacterales is still incomplete. Campylobacterales belong to the class of Epsilonproteobacteria representing a physiologically and ecologically diverse group of bacteria that are rather distinct from the more commonly studied Proteobacteria, such as Escherichia and Salmonella. This review summarises the recent knowledge on distribution and production of AI molecules, as well as possible quorum sensing dependent regulation in the mostly investigated species within the Campylobacterales group: Campylobacter jejuni and Helicobacter pylori.

Related collections

Most cited references 51

Record: found
Abstract: found
Article: not found

Cross-species induction of luminescence in the quorum-sensing bacterium Vibrio harveyi.

B. L. Bassler, E Greenberg, A M Stevens (1997)

Different species of bacteria were tested for production of extracellular autoinducer-like activities that could stimulate the expression of the luminescence genes in Vibrio harveyi. Several species of bacteria, including the pathogens Vibrio cholerae and Vibrio parahaemolyticus, were found to produce such activities. Possible physiological roles for the two V. harveyi detection-response systems and their joint regulation are discussed.

0 comments Cited 171 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Targeting QseC signaling and virulence for antibiotic development.

D Li, Stuart J. Ritchie, Matthew Waldor … (2008)

Many bacterial pathogens rely on a conserved membrane histidine sensor kinase, QseC, to respond to host adrenergic signaling molecules and bacterial signals in order to promote the expression of virulence factors. Using a high-throughput screen, we identified a small molecule, LED209, that inhibits the binding of signals to QseC, preventing its autophosphorylation and consequently inhibiting QseC-mediated activation of virulence gene expression. LED209 is not toxic and does not inhibit pathogen growth; however, this compound markedly inhibits the virulence of several pathogens in vitro and in vivo in animals. Inhibition of signaling offers a strategy for the development of broad-spectrum antimicrobial drugs.

0 comments Cited 141 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Making 'sense' of metabolism: autoinducer-2, LuxS and pathogenic bacteria.

Agnès Vendeville, Karin Heurlier, Kim Hardie … (2005)

Bacteria exploit many mechanisms to communicate with each other and their surroundings. Mechanisms using small diffusible signals to coordinate behaviour with cell density (quorum sensing) frequently contribute to pathogenicity. However, pathogens must also be able to acquire nutrients and replicate to successfully invade their host. One quorum-sensing system, based on the possession of LuxS, bears the unique feature of contributing directly to metabolism, and therefore has the potential to influence both gene regulation and bacterial fitness. Here, we discuss the influence that LuxS and its product, autoinducer-2, have on virulence, relating the current evidence to the preferred niche of the pathogen and the underlying mechanisms involved.