Pseudomonas quinolone signal
The molecule 2-heptyl-3-hydroxy-4-quinolone, also named the Pseudomonas quinolone signal (PQS), has been discovered as an intracellular link between the two major quorum sensing systems of P. aeruginosa; the las and rhl systems.[1] These systems together control expression of virulence factors and play a major role in the formation of biofilms in Pseudomonas aeruginosa. P. aeruginosa is a gram-negative bacteria and opportunistic human pathogen that can cause serious and sometimes fatal infections in humans.[2] Similar to other bacterial species, P. aeruginosa uses quorum sensing (QS) systems to communicate between cells in a population.[1] This allows coordination of gene expression in a population based on changing cell densities, abundance of nutrients, and other environmental factors.
Function[edit]
The functional units of quorum sensing are called autoinducers, which are communicatory molecules that can induce conformist actions among a group. Specific autoinducers are used to influence the group in certain ways, upregulating specific functions while suppressing others. In response to a received signal, the target cell will upregulate the production and release of the same autoinducer. This creates a positive feedback cascade in which all proximal cells will express similar metabolic adjustments, morphological characteristics, and motility.[3]
The Pseudomonas Quinolone Signal (PQS) provides a link between the las and rhI quorum sensing systems.[4] The las system regulates the lasB gene that encodes the lasB elastase enzyme. The lasB elastase enzyme is a secreted protease that functions in causing tissue damage to the host. This exo-protease is able to degrade various plasma proteins such as immunoglobulins, coagulation complement factors, and alpha-proteinase inhibitors.[5] The rhI system regulates the rhII gene which encodes for C4-HSL synthase which plays a significant role in biofilm formation.[6]
Only select bacterium can utilize Quorum sensing in their biofilm production; among the predominant users is P. aeruginosa and the genus Burkholderia to form biofilms. Biofilms are important in all aspects of life and are readily abundant in nearly all environments. They are densely populated with several different survivable microenvironments and can often sort based on optimal metabolic location in accordance with metabolites and byproducts.[7] PQS has also been discovered to play a role in mediating denitrification,[8][9] iron acquisition and cytotoxicity for the cell.[10]
References[edit]
- ^ a b Wilder, Cara N.; Diggle, Stephen P.; Schuster, Martin (2011). ""Cooperation and cheating in Pseudomonas aeruginosa: the roles of the las, rhl and pqs quorum-sensing systems"". The ISME Journal. 5 (8) (published 3 March 2011): 1332–1343. doi:10.1038/ismej.2011.13. ISSN 1751-7370. PMC 3146268. PMID 21368905.
- ^ Bodey, G. P.; Bolivar, R.; Fainstein, V.; Jadeja, L. (1983-03-01). "Infections Caused by Pseudomonas aeruginosa". Clinical Infectious Diseases. 5 (2): 279–313. doi:10.1093/clinids/5.2.279. ISSN 1058-4838.
- ^ Papenfort, Kai; Bassler, Bonnie L. (11 August 2009). "Quorum sensing signal–response systems in Gram-negative bacteria". Nature Reviews Microbiology. 14 (9): 576–588. doi:10.1038/nrmicro.2016.89. ISSN 1740-1534. PMC 5056591. PMID 27510864.
- ^ Calfee, M. Worth; Coleman, James P.; Pesci, Everett C. (2001-09-25). "Interference with Pseudomonas quinolone signal synthesis inhibits virulence factor expression by Pseudomonas aeruginosa". Proceedings of the National Academy of Sciences. 98 (20): 11633–11637. doi:10.1073/pnas.201328498. ISSN 0027-8424. PMC 58781. PMID 11573001.
- ^ Wretlind, Bengt; Pavlovskis, Olǵerts R. (1983-11-01). "Pseudomonas aeruginosa Elastase and Its Role in Pseudomonas Infections". Clinical Infectious Diseases. 5 (Supplement_5): S998–S1004. doi:10.1093/clinids/5.Supplement_5.S998. ISSN 1537-6591.
- ^ Favre-Bonte, S. (2003-09-01). "Biofilm formation by Pseudomonas aeruginosa: role of the C4-HSL cell-to-cell signal and inhibition by azithromycin". Journal of Antimicrobial Chemotherapy. 52 (4): 598–604. doi:10.1093/jac/dkg397. ISSN 1460-2091.
- ^ White, David; Drummond, James; Fuqua, Clay (2012). The Physiology and Biochemistry of Prokaryotes (4 ed.). New York, NY: Oxford University Press. pp. 509–510. ISBN 978-0-19-539304-0.
- ^ Sams, Thomas; Baker, Ysobel; Hodgkinson, James; Gross, Jeremy; Spring, David; Welch, Martin (2016). ""The Pseudomonas Quinolone Signal (PQS)"". Israel Journal of Chemistry. 56 (5): 282–294. doi:10.1002/ijch.201400128. ISSN 0021-2148.
- ^ Toyofuku, Masanori; Nomura, Nobuhiko; Kuno, Eriko; Tashiro, Yosuke; Nakajima, Toshiaki; Uchiyama, Hiroo (2008-12-15). "Influence of the Pseudomonas Quinolone Signal on Denitrification in Pseudomonas aeruginosa". Journal of Bacteriology. 190 (24): 7947–7956. doi:10.1128/jb.00968-08. PMC 2593205. PMID 18931133.
- ^ Abdalla, Maher Y.; Hoke, Traci; Seravalli, Javier; Switzer, Barbara L.; Bavitz, Melissa; Fliege, Jill D.; Murphy, Peter J.; Britigan, Bradley E. (2017-08-18). "Pseudomonas Quinolone Signal Induces Oxidative Stress and Inhibits Heme Oxygenase-1 Expression in Lung Epithelial Cells". Infection and Immunity. 85 (9): 10.1128/iai.00176–17. doi:10.1128/iai.00176-17. PMC 5563587. PMID 28630072.