Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Published online ahead of print on 23 April 2009 as doi:10.1099/mic.0.028001-0
Microbiology 2009;155:2148.

Microbiology (2009), DOI 10.1099/mic.0.028001-0
© 2009 Society for General Microbiology

This Article
Right arrow Full Text (Papers in Press[PDF])
Right arrow All Versions of this Article:
mic.0.028001-0v1
155/7/2148    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Qin, Z.
Right arrow Articles by Tolker-Nielsen, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Qin, Z.
Right arrow Articles by Tolker-Nielsen, T.
Agricola
Right arrow Articles by Qin, Z.
Right arrow Articles by Tolker-Nielsen, T.
Microbiology 0 (2009), mic.0.028001; DOI  10.1099/mic.0.028001-0
© 2009 Society for General Microbiology


Pseudomonas aeruginosa extracellular products inhibit staphylococcal growth and disrupt established biofilms by Staphylococcus epidermidis

Zhiqiang Qin1,4, Liang Yang2, Di Qu3, Soeren Molin2 and Tim Tolker-Nielsen2

1 Medical University of South Carolina;
2 Technical University of Denmark;
3 Shanghai Medical School of Fudan University

ABSTRACT

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. Both S. epidermidis biofilms and planktonic cultures were challenged with P. aeruginosa supernatant cultures overnight. Results indicate 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 has 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 they may provide clues for the development of a novel strategy for controlling S. epidermidis biofilms.

4 E-mail: qinzh{at}musc.edu







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2009 Society for General Microbiology.