Severity of Staphylococcus aureus infection of the skin is associated with inducibility of human beta-defensin 3 but not human beta-defensin 2.
Gram-positive bacteria are the predominant cause of skin infections. Antimicrobial peptides (AMPs) 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 to determining the severity of Gram-positive skin infection. Using real-time PCR, we determined the induction of human beta-defensin 2 (HBD-2), HBD-3, and RNase 7 by comparing healthy and lesional mRNA levels in 32 patients with Gram-positive skin infection. We then examined whether AMP induction differed by disease severity, as measured by number of recurrences and need for surgical drainage in patients with Staphylococcus aureus-positive lesions. We found that HBD-2 and -3, but not RNase 7, mRNA expression was highly induced by Gram-positive bacterial infection in otherwise healthy skin. Less induction 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) than in the respective baseline groups. This suggests that inducibility of HBD-3 influences the severity of Gram-positive skin infection in vivo. The physiological function of HBD-2 induction in this context remains unclear.
Zanger
Philipp
P
Institut für Tropenmedizin, Eberhard Karls Universität, Tübingen, Germany. philipp.zanger@med.uni-tuebingen.de
Holzer
Johannes
J
Schleucher
Regina
R
Scherbaum
Helmut
H
Schittek
Birgit
B
Gabrysch
Sabine
S
D000328:Adult; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology / Q000502:physiology; D006801:Humans; D008297:Male; D012867:Skin / Q000737:chemistry / Q000276:immunology / Q000382:microbiology; D013207:Staphylococcal Skin Infections / Q000276:immunology*; D013211:Staphylococcus aureus / Q000276:immunology / Q000472:pathogenicity; D015854:Up-Regulation / Q000276:immunology / Q000502:physiology; D055815:Young Adult; D023083:beta-Defensins / Q000032:analysis / Q000096:biosynthesis / Q000502:physiology*
C422950:DEFB103A protein, human; C106641:DEFB4A protein, human; D023083:beta-Defensins
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