Abstract
Background
Staphylococcus aureus produces various toxins and enzymes, and its presence can exacerbate skin conditions.
Previous studies have shown that S. aureus is involved in skin deterioration, even in normal tissue. Biofilm strains show much
greater resistance to antimicrobial agents and therefore require a much higher concentration
of biocide than planktonic counterparts.
Objective
As such, alternative strategies and more effective therapeutic agents against biofilm-producing
S. aureus in skin are of great interest. Therefore, we turned our attention to differences
in 50 clinical biofilm strains isolated from human facial skin.
Methods
Based on S. aureus density on facial skin, we divided donors into two groups: relatively low density
(LSG) and high density (HSG). In general, strong biofilm-forming strains were detected
in the HSG donors. Two strains from each of the groups were submitted to gene microarray
analysis to investigate expression differences and confirmed by RT-PCR.
Results
In total, 111 of 7775 genes were differentially expressed between low (SA2 and SA7)
vs. high (SA10 and SA33) biofilm-forming clinical strains. These genes include already
well-known as biofilm formation related genes like icaABCD and lrgAB, and newly identified genes (sdrC, sspBCP) by RT-PCR. Comparison of gene expression differences between the two groups available
at NCBI Gene Expression Omnibus accession number GSE44268.
Conclusion
Our results suggest that S. aureus density in the skin is closely related to biofilm-forming ability, and we have identified
several potential target genes that may be involved in regulating biofilm formation
in situ.
Abbreviations:
BF (biofilm), cfu (colony-forming units), CV (crystal violet), Glc (glucose), HSG (high density of S. aureus detected group), LSG (low density of S. aureus detected group), ORF (open reading frame), TSB (tryptic soy broth)Keywords
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Article info
Publication history
Published online: May 09, 2013
Accepted:
April 10,
2013
Received in revised form:
February 15,
2013
Received:
August 23,
2012
Identification
Copyright
© 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
