Pseudomonas aeruginosa extracellular products inhibit staphylococcal growth, and disrupt established biofilms produced by Staphylococcus epidermidis.
Multiple bacterial species often coexist as communities, and compete for environmental resources. Here, we describe how an opportunistic pathogen, Pseudomonas aeruginosa, uses extracellular products to interact with the nosocomial pathogen Staphylococcus epidermidis. S. epidermidis biofilms and planktonic cultures were challenged with P. aeruginosa supernatant cultures overnight. Results indicated that quorum-sensing-controlled factors from P. aeruginosa supernatant inhibited S. epidermidis growth in planktonic cultures. We also found that P. aeruginosa extracellular products, mainly polysaccharides, disrupted established S. epidermidis biofilms. Cellulase-treated P. aeruginosa supernatant, and supernatant from pelA, pslF and pelApslBCD mutants, which are deficient in polysaccharide biosynthesis, diminished the disruption of S. epidermidis biofilms. In contrast, S. epidermidis supernatant in overnight cultures had no effect on established P. aeruginosa biofilms and planktonic growth. These findings reveal that P. aeruginosa extracellular products are important microbial competition factors that overcome competition with S. epidermidis, and the results may provide clues for the development of a novel strategy for controlling S. epidermidis biofilms.
Qin
Zhiqiang
Z
Division of Infectious Diseases, Department of Medicine, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, USA.|Key Laboratory of Medical Molecular Virology of Ministry of Education and Public Health, Institutes of Biomedical Sciences and Institute of Medical Microbiology, Shanghai Medical School of Fudan University Box 228, Yi Xue Yuan Road 138#, Shanghai 200032, PR China.|Centre for Biomedical Microbiology, BioCentrum-DTU, Technical University of Denmark, DK-2800 Lyngby, Denmark.
Yang
Liang
L
Centre for Biomedical Microbiology, BioCentrum-DTU, Technical University of Denmark, DK-2800 Lyngby, Denmark.
Qu
Di
D
Key Laboratory of Medical Molecular Virology of Ministry of Education and Public Health, Institutes of Biomedical Sciences and Institute of Medical Microbiology, Shanghai Medical School of Fudan University Box 228, Yi Xue Yuan Road 138#, Shanghai 200032, PR China.
Molin
Soeren
S
Centre for Biomedical Microbiology, BioCentrum-DTU, Technical University of Denmark, DK-2800 Lyngby, Denmark.
Tolker-Nielsen
Tim
T
Department of International Health, Immunology and Microbiology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.|Centre for Biomedical Microbiology, BioCentrum-DTU, Technical University of Denmark, DK-2800 Lyngby, Denmark.
D018441:Biofilms; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism; D015169:Colony Count, Microbial; D011133:Polysaccharide-Lyases / Q000172:deficiency; D011135:Polysaccharides, Bacterial / Q000096:biosynthesis; D011550:Pseudomonas aeruginosa / Q000378:metabolism*; D015363:Quinolones / Q000378:metabolism; D053038:Quorum Sensing; D013212:Staphylococcus epidermidis / Q000502:physiology*
C407944:2-heptyl-3-hydroxy-4-quinolone; D011135:Polysaccharides, Bacterial; D015363:Quinolones; D002265:Carboxylic Ester Hydrolases; C432003:N-acyl homoserine lactonase; D011133:Polysaccharide-Lyases; C023911:pectate lyase