User:Cathalgarvey/SpecialBookPages/BacterialQuorumSensing
Quorum sensing is a system of stimulus and response correlated to population density. Many species of
Quorum sensing can function as a decision-making process in any decentralized system, as long as individual components have: (a) a means of assessing the number of other components they interact with and (b) a standard response once a threshold number of components is detected.
Quorum quenching
Quorum quenching may be achieved by degrading the signalling molecule.[1][2] Using a KG medium, quorum quenching bacteria can be readily isolated from various environments including that which has previously been considered as unculturable.[2] Recently, a well-studied quorum quenching bacteria has been isolated and its AHL degradation kinetic has been studied by using rapid resolution liquid chromatography (RRLC).[3]
Bacteria
Some of the best-known examples of quorum sensing come from studies of
Mechanism
Bacteria that use quorum sensing constantly produce and secrete certain
Examples
Vibrio fischeri
Quorum sensing was first observed in
Escherichia coli
In the Gram-negative bacteria
E. coli and Salmonella enterica do not produce AHL signals commonly found in other Gram-negative bacteria. However, they have a receptor that detects AHLs from other bacteria and change their gene expression in accordance with the presence of other "quorate" populations of Gram-negative bacteria.[6]
Salmonella enterica
Salmonella encodes a LuxR homolog, SdiA, but does not encode an AHL synthase. SdiA detects AHLs produced by other species of bacteria including Aeromonas hydrophila, Hafnia alvei, and Yersinia enterocolitica.[7] When AHL is detected, SdiA regulates the rck operon on the Salmonella virulence plasmid (pefI-srgD-srgA-srgB-rck-srgC) and a single gene horizontal acquisition in the chromosome srgE.[8][9] Salmonella does not detect AHL when passing through the gastrointestinal tracts of several animal species, suggesting that the normal microbiota does not produce AHLs. However, SdiA does become activated when Salmonella transits through turtles colonized with Aeromonas hydrophila or mice infected with Yersinia enterocolitica.[10][11] Therefore, Salmonella appears to use SdiA to detect the AHL production of other pathogens rather than the normal gut flora.
Pseudomonas aeruginosa
The opportunistic bacteria
Acinetobacter sp.
It has recently been found that Acinetobacter sp. also show quorum sensing activity. This bacterium, an emerging pathogen, produces AHLs.[15] Interestingly, Acinetobacter sp. shows both quorum sensing and quorum quenching activity. It produces AHLs and also, it can degrade the AHL molecules as well.[15]
Aeromonas sp.
This bacterium used to be considered a fish pathogen, but it has recently emerged as a human pathogen.[citation needed] Aeromonas sp. have been isolated from various infected sites from patients (bile, blood, peritoneal fluid, pus, stool and urine). All isolates produced the two principal AHLs, N-butanoylhomoserine lactone (C4-HSL) and N-hexanoyl homoserine lactone (C6-HSL). It has been documented that Aeromonas sobria has produced C6-HSL and two additional AHLs with N-acyl side chain longer than C6.[16]
Molecules involved in quorum sensing
Three-dimensional structures of proteins involved in quorum sensing were first published in 2001, when the
Certain bacteria can produce enzymes called lactonases that can target and inactivate AHLs.
Evolution
Sequence analysis
The majority of quorum sensing systems that fall under the "two-gene" (an autoinducer synthase coupled with a receptor molecule) paradigm as defined by the
Although examples of horizontal gene transfer are apparent in LuxI, LuxR, and LuxS phylogenies, they are relatively rare. This result is in line with the observation that quorum sensing genes tend to control the expression of a wide array of genes scattered throughout the bacterial chromosome. A recent acquisition by horizontal gene transfer would be unlikely to have integrated itself to this degree. Given that the majority of autoinducer–synthase/receptor occurs in tandem in bacterial genomes, it is also rare that they switch partners and so pairs tend to co-evolve.[21]
The phylogeny of quorum sensing genes in Gammaproteobacteria (which includes Pseudomonas aeruginosa and Escherichia coli) is especially interesting.[according to whom?] The LuxI/LuxR genes form a functional pair, with LuxI as the auto-inducer synthase and LuxR as the receptor. Gamma Proteobacteria are unique in possessing quorum sensing genes, which, although functionally similar to the LuxI/LuxR genes, have a markedly divergent sequence.[21] This family of quorum-sensing homologs may have arisen in the gamma Proteobacteria ancestor, although the cause of their extreme sequence divergence yet maintenance of functional similarity has yet to be explained. In addition, species that employ multiple discrete quorum sensing systems are almost all members of the gamma Proteobacteria, and evidence of horizontal transfer of quorum sensing genes is most evident in this class.[20][21]
Controversy
As quorum sensing implies a cooperative behavior, this concept has been challenged by the evolutionary implication of cooperative cheaters. This is circumvented by the concept of diffusion sensing, which has been an alternative and complementary model to quorum sensing. However, both explanations face the problems of signalling in either complex (multiple species sharing the same space) or simple (one single cell confined to a limited volume) environments where the spatial distribution of the cells can be more important for sensing than the cell population density. A new model, efficiency sensing, which takes into account both problematics, population density and spatial confinement, has been proposed as an alternative.[22] One of the probable reasons for controversy is that current terminologies (quorum sensing, diffusion sensing, efficiency sensing) all imply an understanding of the motives and benefits of the process, and may be observed to apply under some circumstances but not others. Perhaps a sensible resolution to these controversies could be to return the terminology of the process to autoinduction, as originally described by Hastings and coworkers, as this term does not imply understanding of the intent(s) or benefit(s) of the process.
Anti-quorum sensing medical treatments
Today, about 70% of the bacteria that cause infections are resistant to at least one of the drugs most commonly used for treatment.[dubious – discuss] Some organisms are resistant to all approved antibiotics and can be treated only with experimental and potentially toxic drugs. A substancial increase in resistance of bacteria that cause community-acquired infections has also been documented, especially in the staphylococci and pneumococci, which are prevalent causes of disease and mortality. In a recent study, 25% of bacterial pneumonia cases were shown to be resistant to penicillin, and an additional 25% of cases were resistant to more than one antibiotic.[citation needed]
The current state of antibiotic affairs is due to the manner in which existing antibiotics work. All current antibiotics aim to kill the individual bacteria in one manner or another (by inhibiting synthesis of new bacteria, usually).[citation needed] This environmental pressure activates the evolutionary mechanisms that select for resistant strains. In other words, bacteria that are not resistant to the antibiotic are killed off, leaving the resistant organisms to multiply unchecked without competition. This is why resistant strains spread so rapidly and occur so frequently.
Recent research into quorum sensing systems has produced compounds that can disrupt the bacteria's ability to communicate, thereby disabling or diminishing the bacteria's ability to become pathogenic. Therefore, the body is not compromised by cell damage, inflammation, toxicity, or other detrimental effects of the bacteria. This gives the body time to eradicate the bacteria naturally through normal immune system functions.
The advantage of the anti-quorum sensing approach to controlling infection is that there are few evolutionary forces that select for resistance—there is little in the process that would create resistant strains. Since the compounds kill none of the bacteria, any resistant mutations must compete with living, non-resistant individuals. In other words, there is no survival advantage to the resistant mutations, and natural selection does not come into play. Resistant strains will be unlikely to occur.[23]
- PMID 21385437.)
{{cite journal}}
: CS1 maint: date and year (link) CS1 maint: unflagged free DOI (link - ^ PMID 18946694.)
{{cite journal}}
: CS1 maint: date and year (link - PMID 20376561.)
{{cite journal}}
: CS1 maint: date and year (link - PMID 11544353.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 5473898.
- PMID 15130116.
- PMID 11544237.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 9495757.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 12562806.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 18665275.)
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link - PMID 19820103.)
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link - PMID 11807075.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - ISBN 978-1904455196. [http://www.horizonpress.com/pseudo.)
{{cite book}}
:|author=
has generic name (help - PMID 16339933.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - ^ PMID 21385437.)
{{cite journal}}
: CS1 maint: date and year (link) CS1 maint: unflagged free DOI (link - )
- PMID 11435117.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 11823863.)
{{cite journal}}
: Check|url=
value (help)CS1 maint: multiple names: authors list (link - PMID 15456522.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link - ^ PMID 11496014.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - ^ PMID 15014168.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 17304251.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - ^ Quorumex