title: Biofilms and type III secretion are not mutually exclusive in Pseudomonas aeruginosa.
abstract: Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen that causes acute and chronic infections in immunocompromised individuals. It is also a model organism for bacterial biofilm formation. Acute infections are often associated with planktonic or free-floating cells, high virulence and fast growth. Conversely, chronic infections are often associated with the biofilm mode of growth, low virulence and slow growth that resembles that of planktonic cells in stationary phase. Biofilm formation and type III secretion have been shown to be reciprocally regulated, and it has been suggested that factors related to acute infection may be incompatible with biofilm formation. In a previous proteomic study of the interrelationships between planktonic cells, colonies and continuously grown biofilms, we showed that biofilms under the growth conditions applied are more similar to planktonic cells in exponential phase than to those in stationary phase. In the current study, we investigated how these conditions influence the production of virulence factors using a transcriptomic approach. Our results show that biofilms express the type III secretion system, whereas planktonic cells do not. This was confirmed by the detection of PcrV in the cellular and secreted fractions of biofilms, but not in those of planktonic cells. We also detected the type III effector proteins ExoS and ExoT in the biofilm effluent, but not in the supernatants of planktonic cells. Biofilm formation and type III secretion are therefore not mutually exclusive in P. aeruginosa, and biofilms could play a more active role in virulence than previously thought.
authors.affiliation: Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK.
authors.forename: H
authors.initials: H
authors.lastname: Mikkelsen
authors.affiliation: Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK.
authors.forename: N J
authors.initials: NJ
authors.lastname: Bond
authors.affiliation: ChemoMetec A/S, Gydevang 43, DK-3450 Alleroed, Denmark.
authors.forename: M E
authors.initials: ME
authors.lastname: Skindersoe
authors.affiliation: Department of International Health, Immunology and Microbiology, Faculty of Health, Panum Institute, University of Copenhagen, DK-2200 Copenhagen N, Denmark.
authors.forename: M
authors.initials: M
authors.lastname: Givskov
authors.affiliation: Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK.
authors.forename: K S
authors.initials: KS
authors.lastname: Lilley
authors.affiliation: Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK.
authors.forename: M
authors.initials: M
authors.lastname: Welch
mesh_terms: D001426:Bacterial Proteins / Q000378:metabolism; D018441:Biofilms / Q000254:growth & development*; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D020411:Oligonucleotide Array Sequence Analysis; D011550:Pseudomonas aeruginosa / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism*; D012329:RNA, Bacterial / Q000378:metabolism; D037521:Virulence Factors / Q000096:biosynthesis*
chemical_list: D001426:Bacterial Proteins; D012329:RNA, Bacterial; D037521:Virulence Factors