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Res Microbiol. 2011 Jun;162(5):535-41. doi: 10.1016/j.resmic.2011.03.008. Epub 2011 Mar 12.

Extracellular DNA-dependent biofilm formation by Staphylococcus epidermidis RP62A in response to subminimal inhibitory concentrations of antibiotics.

Author information

1
Department of Oral Biology, New Jersey Dental School, Medical Science Building, Room C636, 185 S. Orange Ave., Newark, NJ 07103, USA. kaplanjb@umdnj.edu

Abstract

We measured the ability of Staphylococcus epidermidis to form biofilms in the presence of subminimal inhibitory concentrations (sub-MICs) of vancomycin, tigecycline, linezolid and novobiocin. Six strains that produce different amounts of biofilm were tested. The three strains that produced the highest amounts of biofilm exhibited steady-state or decreased biofilm formation in the presence of sub-MIC antibiotics, whereas the three strains that produced lower amounts of biofilm exhibited up to 10-fold-increased biofilm formation in the presence of sub-MIC antibiotics. In two of the inducible strains (9142 and 456a), antibiotic-induced biofilm formation was inhibited by dispersin B, an enzyme that degrades poly-N-acetylglucosamine (PNAG) biofilm polysaccharide. In the third inducible strain (RP62A), dispersin B inhibited biofilm formation in response to sub-MIC vancomycin, but not to sub-MIC tigecycline. In contrast, DNase I efficiently inhibited biofilm formation by strain RP62A in response to sub-MIC tigecycline and vancomycin. DNase I had no effect on antibiotic-induced biofilm formation in strains 9142 and 456a. Our findings indicate that antibiotic-induced biofilm formation in S. epidermidis is both strain- and antibiotic-dependent and that S. epidermidis RP62A utilizes an extracellular DNA-dependent mechanism to form biofilms in response to sub-MIC antibiotics.

PMID:
21402153
PMCID:
PMC3109171
DOI:
10.1016/j.resmic.2011.03.008
[Indexed for MEDLINE]
Free PMC Article

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