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Microbiology 154 (2008), 2827-2836; DOI  10.1099/mic.0.2007/015768-0
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Microbiology 154 (2008), 2827-2836; DOI  10.1099/mic.0.2007/015768-0
© 2008 Society for General Microbiology

The role of {sigma}B in persistence of Staphylococcus epidermidis foreign body infection

Valerie Pintens1, Caroline Massonet1, Rita Merckx1, Stefaan Vandecasteele2, Willy E. Peetermans3, Johannes K.-M. Knobloch4 and Johan Van Eldere1

1 Department of Medical Diagnostics, Laboratory of Clinical and Experimental Microbiology, KULeuven, UZ Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium
2 Department of Internal Medicine and Infectious Diseases, AZ Sint-Jan AV, Ruddershove 10, B-8000 Brugge, Belgium
3 Department of Internal Medicine, UZ Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium
4 Institut für Medizinische Mikrobiologie und Hygiene, Universität Lübeck, 23538 Lübeck, Germany

Correspondence
Valerie Pintens
valerie.pintens{at}rega.kuleuven.be

Staphylococcal biofilm formation depends on the transcription factor {sigma}B. We further investigated the role of {sigma}B in biofilm formation and persistence in vitro and in vivo in a subcutaneous rat model. As expected, expression of all {sigma}B operon genes was transiently higher in the first 6 h of biofilm formation compared to planktonic bacteria, concurrent with a temporary upregulation of icaA and aap expression. However, we also observed a second upregulation of sigB expression in biofilm more than 2 days old without upregulation of icaA or aap. Biofilm formation by Staphylococcus epidermidis strains 8400 and 1457 was compared to that of isogenic mutants with inactivation of rsbU, of rsbUVW and of the entire {sigma}B operon. Both wild-type strains and the constitutively sigB-expressing rsbUVW mutant showed a strong biofilm-positive phenotype. The rsbUVW mutant biofilm was, however, thinner and more evenly spread than the wild-type biofilm. Inactivation of SigB in the rsbUVWsigB mutant or mutation of the positive regulator RsbU reduced both the number of sessile bacteria and polysaccharide intercellular adhesin (PIA) synthesis. These differences between the wild-types and their respective mutants appeared after 6 h in in vitro biofilms but only after 4 days in in vivo biofilms. Our results provide additional evidence for a role for {sigma}B in biofilm formation. They also suggest a role for {sigma}B in biofilm maturation and stability that is independent of PIA or accumulation-associated protein (Aap) and point to significant differences in the temporal development between in vitro and in vivo biofilms.


Abbreviations: CLSM, confocal laser-scanning microscopy; CoNS, coagulase-negative staphylococci; FBI, foreign body infection; gDNA, genomic DNA; PIA, polysaccharide intercellular adhesin; SEM, scanning electron microscopy




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M. Shahrooei, V. Hira, B. Stijlemans, R. Merckx, P. W. M. Hermans, and J. Van Eldere
Inhibition of Staphylococcus epidermidis Biofilm Formation by Rabbit Polyclonal Antibodies against the SesC Protein
Infect. Immun., September 1, 2009; 77(9): 3670 - 3678.
[Abstract] [Full Text] [PDF]




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