Gene expression during S. epidermidis biofilm formation on biomaterials

Biomaterial‐centered infections are initiated by adhesion of bacteria to an implant, followed by colonization and mature biofilm formation. Staphylococcus epidermidis is commonly identified as the cause of these device‐centered infections. This study used an in vitro model to evaluate temporal chang...

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Veröffentlicht in:Journal of biomedical materials research. Part A 2012-11, Vol.100A (11), p.2863-2869
Hauptverfasser: Patel, Jasmine D., Colton, Erica, Ebert, Michael, Anderson, James M.
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Sprache:eng
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Zusammenfassung:Biomaterial‐centered infections are initiated by adhesion of bacteria to an implant, followed by colonization and mature biofilm formation. Staphylococcus epidermidis is commonly identified as the cause of these device‐centered infections. This study used an in vitro model to evaluate temporal changes in the expression of genes—icaADBC, agrBDCA, aap, and atle—that have been identified to play a role in the pathogenesis of S. epidermidis infections. Real‐time reverse transcription–polymerase chain reaction was used to determine changes in gene expression from S epidermidis biofilm grown on polyurethanes (Elasthane 80A, hydrophobic) modified with polyethylene oxide (Elasthane 80A–6PEO, hydrophilic) and fluorocarbon (Elasthane 80A–6F, hydrophobic). In vitro expression of the ica locus, which is involved in initial adhesion and intracellular aggregation, increased up to 100‐fold from 2 to 48 h, whereas gene expression for autolysin AtlE decreased slightly from 2 to 12 h, followed by a 10‐fold increase by 48 h. Upregulation of the aap gene associated with bacterial accumulation and the agr quorum‐sensing system was observed during biofilm formation over 48 h. In addition, no correlation was observed between S. epidermidis gene expression and biomaterial surface chemistry. This study used an in vitro model to demonstrate that enhanced expression of the atle, aap, agr, and ica genes plays an important role in initial foreign body colonization and potentially in the establishment of a device‐associated infection. © 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 100A:2863–2869, 2012.
ISSN:1549-3296
1552-4965
DOI:10.1002/jbm.a.34221