Biofilms and type III secretion are not mutually exclusive in Pseudomonas aeruginosa
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Biofilms and type III secretion are not mutually exclusive in Pseudomonas aeruginosa. / Mikkelsen, H; Bond, N J; Skindersoe, M E; Givskov, M; Lilley, K S; Welch, M.
In: Microbiology, Vol. 155, No. Pt 3, 2009, p. 687-98.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Biofilms and type III secretion are not mutually exclusive in Pseudomonas aeruginosa
AU - Mikkelsen, H
AU - Bond, N J
AU - Skindersoe, M E
AU - Givskov, M
AU - Lilley, K S
AU - Welch, M
N1 - Keywords: Bacterial Proteins; Biofilms; Gene Expression Profiling; Gene Expression Regulation, Bacterial; Oligonucleotide Array Sequence Analysis; Pseudomonas aeruginosa; RNA, Bacterial; Virulence Factors
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
U2 - 10.1099/mic.0.025551-0
DO - 10.1099/mic.0.025551-0
M3 - Journal article
C2 - 19246740
VL - 155
SP - 687
EP - 698
JO - Microbiology
JF - Microbiology
SN - 1350-0872
IS - Pt 3
ER -
ID: 21331853