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dc.contributor.authorHentzer, Morten
dc.contributor.authorWu, Hong
dc.contributor.authorAndersen, Jens B.
dc.contributor.authorRiedel, Kathrin
dc.contributor.authorRasmussen, Thomas B.
dc.contributor.authorBagge, Niels
dc.contributor.authorKumar, Naresh
dc.contributor.authorSchembri, Mark A.
dc.contributor.authorSong, Zhijun
dc.contributor.authorKristoffersen, Peter
dc.contributor.authorManefield, Mike
dc.contributor.authorCosterton, J. William
dc.contributor.authorMolin, Søren
dc.contributor.authorEberl, Leo
dc.contributor.authorSteinberg, Peter
dc.contributor.authorKjelleberg, Staffan
dc.contributor.authorHøiby, Niels
dc.contributor.authorGivskov, Michael
dc.date.accessioned2017-08-08T22:34:31Z
dc.date.available2017-08-08T22:34:31Z
dc.date.issued2003-08
dc.identifier.citationHentzer M, Wu H, Andersen JB, Riedel K, Rasmussen TB, Bagge N, Kumar N, Schembri MA, Song Z, Kristoffersen P, Manefield M, Costerton JW, Molin S, Eberl L, Steinberg P, Kjelleberg S, Hoiby N, Givskov M, "Attenuation of Pseudomonas aeruginosa virulence by quorum sensing inhibitors," EMBO J., 22(15):3803–3815 (2003).en_US
dc.identifier.issn0261-4189
dc.identifier.urihttps://scholarworks.montana.edu/xmlui/handle/1/13487
dc.description.abstractTraditional treatment of infectious diseases is based on compounds that kill or inhibit growth of bacteria. A major concern with this approach is the frequent development of resistance to antibiotics. The discovery of communication systems (quorum sensing systems) regulating bacterial virulence has afforded a novel opportunity to control infectious bacteria without interfering with growth. Compounds that can override communication signals have been found in the marine environment. Using Pseudomonas aeruginosa PAO1 as an example of an opportunistic human pathogen, we show that a synthetic derivate of natural furanone compounds can act as a potent antagonist of bacterial quorum sensing. We employed GeneChip microarray technology to identify furanone target genes and to map the quorum sensing regulon. The transcriptome analysis showed that the furanone drug specifically targeted quorum sensing systems and inhibited virulence factor expression. Application of the drug to P. aeruginosa biofilms increased bacterial susceptibility to tobramycin and SDS. In a mouse pulmonary infection model, the drug inhibited quorum sensing of the infecting bacteria and promoted their clearance by the mouse immune response.en_US
dc.titleAttenuation of Pseudomonas aeruginosa virulence by quorum sensing inhibitorsen_US
dc.typeArticleen_US
mus.citation.extentfirstpage3803en_US
mus.citation.extentlastpage3815en_US
mus.citation.issue15en_US
mus.citation.journaltitleEMBO Journalen_US
mus.citation.volume22en_US
mus.identifier.categoryEngineering & Computer Scienceen_US
mus.identifier.doi10.1093/emboj/cdg366en_US
mus.relation.collegeCollege of Engineeringen_US
mus.relation.departmentCenter for Biofilm Engineering.en_US
mus.relation.departmentChemical & Biological Engineering.en_US
mus.relation.departmentChemical Engineering.en_US
mus.relation.universityMontana State University - Bozemanen_US
mus.relation.researchgroupCenter for Biofilm Engineering.en_US
mus.data.thumbpage4en_US


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