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Infection and Immunity, September 2009, p. 3670-3678, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.01464-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Inhibition of Staphylococcus epidermidis Biofilm Formation by Rabbit Polyclonal Antibodies against the SesC Protein{triangledown}

Mohammad Shahrooei,1* Vishal Hira,2 Benoit Stijlemans,3 Rita Merckx,1 Peter W. M. Hermans,4 and Johan Van Eldere1

Laboratory of Medical Microbiology, Department of Medical Diagnostic Sciences, KU Leuven, U.Z. Gasthuisberg, Herestraat 49 CDG 8th floor, B-3000 Leuven, Belgium,1 Department of Pediatrics, Erasmus MC—Sophia Children's Hospital, Rotterdam, The Netherlands,2 Laboratory of Cellular and Molecular Immunology, VIB Department of Molecular and Cellular Interactions, Vrije Universiteit Brussel (VUB), Building E, Level 8, Pleinlaan 2, B-1050 Brussels, Belgium,3 Department of Pediatrics, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands4

Received 1 December 2008/ Returned for modification 22 January 2009/ Accepted 7 June 2009

Several well-studied proteins with defined roles in Staphylococcus epidermidis biofilm formation are LPXTG motif-containing proteins. Here, we investigate the possible use of the LPXTG motif-containing protein SesC (S. epidermidis surface protein C; accession no. NP_765787) as a target for antibodies to prevent biofilm formation. In vitro and in a in vivo rat model of catheter infection, gene and protein expression analysis showed that SesC is expressed more strongly in biofilm-associated cells than in planktonic cells and is expressed particularly during the late phase of in vivo biofilm formation. Polyclonal rabbit antibodies raised against SesC reduced the fibrinogen-binding ability of S. epidermidis RP62A and Staphylococcus aureus RN4220 transformants expressing SesC, inhibited in vitro biofilm formation by S. epidermidis strains 10b and 1457, and significantly reduced the numbers of bacteria in a 1-day-old in vivo biofilm (P < 0.001, one-way analysis of variance). Our findings revealed that SesC is a promising target for prevention and treatment of S. epidermidis biofilms because it affects both the primary attachment and biofilm accumulation phases. The precise role of SesC in biofilm formation remains to be identified.

* Corresponding author. Mailing address: Afd. Exp. laboratoriumgeneeskunde, O. & N., Herestraat 49-bus 819, BE-3000 Leuven, Belgium. Phone: 32 16 34 62 74. Fax: 32 16 34 62 75. E-mail: Mohammad.Shahrooei{at}med.kuleuven.be

{triangledown} Published ahead of print on 15 June 2009.

Editor: A. Camilli

Infection and Immunity, September 2009, p. 3670-3678, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.01464-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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