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Semin Immunopathol. 2012 Mar;34(2):201-14. doi: 10.1007/s00281-011-0296-2. Epub 2011 Nov 19.

Molecular basis of Staphylococcus epidermidis infections.

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  • 1Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, NIAID, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA. motto@niaid.nih.gov

Abstract

Staphylococcus epidermidis is the most important member of the coagulase-negative staphylococci and one of the most abundant colonizers of human skin. While for a long time regarded as innocuous, it has been identified as the most frequent cause of device-related infections occurring in the hospital setting and is therefore now recognized as an important opportunistic pathogen. S. epidermidis produces a series of molecules that provide protection from host defenses. Specifically, many proteins and exopolymers, such as the exopolysaccharide PIA, contribute to biofilm formation and inhibit phagocytosis and the activity of human antimicrobial peptides. Furthermore, recent research has identified a family of pro-inflammatory peptides in S. epidermidis, the phenol-soluble modulins (PSMs), which have multiple functions in immune evasion and biofilm development, and may be cytolytic. However, in accordance with the relatively benign relationship that S. epidermidis has with its host, production of aggressive members of the PSM family is kept at a low level. Interestingly, in contrast to S. aureus with its large arsenal of toxins developed for causing infection in the human host, most if not all "virulence factors" of S. epidermidis appear to have original functions in the commensal lifestyle of this bacterium.

PMID:
22095240
[PubMed - indexed for MEDLINE]
PMCID:
PMC3272124
Free PMC Article
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