IRIS publication 102259661
The Pseudomonas quinolone signal (PQS), and its precursor HHQ, modulate interspecies and interkingdom behaviour
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TY - JOUR - Reen, FJ,Mooij, MJ,Holcombe, LJ,McSweeney, CM,McGlacken, GP,Morrissey, JP,O'Gara, F - 2011 - January - Fems Microbiology Ecology - The Pseudomonas quinolone signal (PQS), and its precursor HHQ, modulate interspecies and interkingdom behaviour - Validated - () - interspecies/interkingdom Pseudomonas quinolone signal PQS HHQ biofilm motility TO-CELL COMMUNICATION QUORUM-SENSING MOLECULES CYSTIC-FIBROSIS PATIENTS CANDIDA-ALBICANS GENE-EXPRESSION BURKHOLDERIA-PSEUDOMALLEI AERUGINOSA AUTOINDUCER PROTEOMIC ANALYSIS BACTERIAL-CELL HUMAN PATHOGEN - 77 - 413 - 428 - The Pseudomonas quinolone signal (PQS), and its precursor 2-heptyl-4-quinolone (HHQ), play a key role in coordinating virulence in the important cystic fibrosis pathogen Pseudomonas aeruginosa. The discovery of HHQ analogues in Burkholderia and other microorganisms led us to investigate the possiblity that these compounds can influence interspecies behaviour. We found that surface-associated phenotypes were repressed in Gram-positive and Gram-negative bacteria as well as in pathogenic yeast in response to PQS and HHQ. Motility was repressed in a broad range of bacteria, while biofilm formation in Bacillus subtilis and Candida albicans was repressed in the presence of HHQ, though initial adhesion was unaffected. Furthermore, HHQ exhibited potent bacteriostatic activity against several Gram-negative bacteria, including pathogenic Vibrio vulnificus. Structure-function analysis using synthetic analogues provided an insght into the molecular properties that underpin the ability of these compounds to influence microbial behaviour, revealing the alkyl chain to be fundamental. Defining the influence of these molecules on microbial-eukaryotic-host interactions will facilitate future therapeutic strategies which seek to combat microorganisms that are recalcitrant to conventional antimicrobial agents. - DOI 10.1111/j.1574-6941.2011.01121.x DA - 2011/01 ER -
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@article{V102259661, = {Reen, FJ and Mooij, MJ and Holcombe, LJ and McSweeney, CM and McGlacken, GP and Morrissey, JP and O'Gara, F }, = {2011}, = {January}, = {Fems Microbiology Ecology}, = {The Pseudomonas quinolone signal (PQS), and its precursor HHQ, modulate interspecies and interkingdom behaviour}, = {Validated}, = {()}, = {interspecies/interkingdom Pseudomonas quinolone signal PQS HHQ biofilm motility TO-CELL COMMUNICATION QUORUM-SENSING MOLECULES CYSTIC-FIBROSIS PATIENTS CANDIDA-ALBICANS GENE-EXPRESSION BURKHOLDERIA-PSEUDOMALLEI AERUGINOSA AUTOINDUCER PROTEOMIC ANALYSIS BACTERIAL-CELL HUMAN PATHOGEN}, = {77}, pages = {413--428}, = {{The Pseudomonas quinolone signal (PQS), and its precursor 2-heptyl-4-quinolone (HHQ), play a key role in coordinating virulence in the important cystic fibrosis pathogen Pseudomonas aeruginosa. The discovery of HHQ analogues in Burkholderia and other microorganisms led us to investigate the possiblity that these compounds can influence interspecies behaviour. We found that surface-associated phenotypes were repressed in Gram-positive and Gram-negative bacteria as well as in pathogenic yeast in response to PQS and HHQ. Motility was repressed in a broad range of bacteria, while biofilm formation in Bacillus subtilis and Candida albicans was repressed in the presence of HHQ, though initial adhesion was unaffected. Furthermore, HHQ exhibited potent bacteriostatic activity against several Gram-negative bacteria, including pathogenic Vibrio vulnificus. Structure-function analysis using synthetic analogues provided an insght into the molecular properties that underpin the ability of these compounds to influence microbial behaviour, revealing the alkyl chain to be fundamental. Defining the influence of these molecules on microbial-eukaryotic-host interactions will facilitate future therapeutic strategies which seek to combat microorganisms that are recalcitrant to conventional antimicrobial agents.}}, = {DOI 10.1111/j.1574-6941.2011.01121.x}, source = {IRIS} }
Data as stored in IRIS
AUTHORS | Reen, FJ,Mooij, MJ,Holcombe, LJ,McSweeney, CM,McGlacken, GP,Morrissey, JP,O'Gara, F | ||
YEAR | 2011 | ||
MONTH | January | ||
JOURNAL_CODE | Fems Microbiology Ecology | ||
TITLE | The Pseudomonas quinolone signal (PQS), and its precursor HHQ, modulate interspecies and interkingdom behaviour | ||
STATUS | Validated | ||
TIMES_CITED | () | ||
SEARCH_KEYWORD | interspecies/interkingdom Pseudomonas quinolone signal PQS HHQ biofilm motility TO-CELL COMMUNICATION QUORUM-SENSING MOLECULES CYSTIC-FIBROSIS PATIENTS CANDIDA-ALBICANS GENE-EXPRESSION BURKHOLDERIA-PSEUDOMALLEI AERUGINOSA AUTOINDUCER PROTEOMIC ANALYSIS BACTERIAL-CELL HUMAN PATHOGEN | ||
VOLUME | 77 | ||
ISSUE | |||
START_PAGE | 413 | ||
END_PAGE | 428 | ||
ABSTRACT | The Pseudomonas quinolone signal (PQS), and its precursor 2-heptyl-4-quinolone (HHQ), play a key role in coordinating virulence in the important cystic fibrosis pathogen Pseudomonas aeruginosa. The discovery of HHQ analogues in Burkholderia and other microorganisms led us to investigate the possiblity that these compounds can influence interspecies behaviour. We found that surface-associated phenotypes were repressed in Gram-positive and Gram-negative bacteria as well as in pathogenic yeast in response to PQS and HHQ. Motility was repressed in a broad range of bacteria, while biofilm formation in Bacillus subtilis and Candida albicans was repressed in the presence of HHQ, though initial adhesion was unaffected. Furthermore, HHQ exhibited potent bacteriostatic activity against several Gram-negative bacteria, including pathogenic Vibrio vulnificus. Structure-function analysis using synthetic analogues provided an insght into the molecular properties that underpin the ability of these compounds to influence microbial behaviour, revealing the alkyl chain to be fundamental. Defining the influence of these molecules on microbial-eukaryotic-host interactions will facilitate future therapeutic strategies which seek to combat microorganisms that are recalcitrant to conventional antimicrobial agents. | ||
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DOI_LINK | DOI 10.1111/j.1574-6941.2011.01121.x | ||
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