Artikel
Inducibility of the antimicrobial peptides RNase7, HBD-2 and HBD-3 and its influence on clinical outcome of Staphylococcus aureus-positive skin infections
Induzierbarkeit der antimikrobiellen Peptide RNase7, HBD-2 and HBD-3 und ihr Einfluss auf den klinischen Verlauf von durch Staphyloccus aureus verursachten Hautinfektionen
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Autoren
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P. Zanger
- Universität Tübingen, Institut für Tropenmedizin, Tübingen, Germany
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J. Holzer
- Universität Tübingen, Institut für Tropenmedizin, Tübingen, Germany
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R. Schleucher
- Tropmed-Ruhr, Bochum, Germany
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H. Scherbaum
- Tropenklinik, Paul-Lechler-Krankenhaus, Tübingen, Germany
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B. Schittek
- Universität Tübingen, Hautklinik, Tübingen, Germany
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S. Gabrysch
- Universtität Heidelberg, Institut für Public Health, Heidelberg, Germany
| Veröffentlicht: | 2. Juni 2010 |
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Gliederung
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Objectives: Gram-positive bacteria are the predominant cause of skin infections. Antimicrobial peptides (AMP) are believed to be of major importance in skin's innate defense against these pathogens. This study aimed at providing clinical evidence for the contribution of AMP inducibility in determining the severity of gram-positive skin infection.
Methods: Using real-time-PCR we determined inducibility of human β-defensins (HBD) -2, HBD-3 and RNase 7 by comparing healthy and lesional mRNA levels in 32 patients with gram-positive skin infection. We examined whether AMP inducibility differed by disease severity, as measured by number of recurrences and need for surgical drainage in patients with S. aureus-positive lesions.
Results: HBD-2 and -3, but not RNase 7 mRNA expression was highly inducible by gram-positive infection in previously healthy skin. Lower inducibility of HBD-3, but not HBD-2, was associated with more severe S. aureus skin infection: HBD-3 mRNA levels were 11.4 times lower in patients with more than 6 recurrences (p=0.01) and 8.8 times lower in patients reporting surgical drainage (p=0.01) as compared to baseline severity.
(Figure 1 [Fig. 1])
Conclusions: Inducibility of HBD-3 appears to be a determinant of the severity of gram-positive skin infections in vivo. The physiological function of HBD-2 induction in this context remains unclear.
