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Endogenous antimicrobial peptides and skin infections in atopic dermatitis
Peck Y Ong1, Takaaki Ohtake, Corinne Brandt
1Division of Allergy and Immunology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA.
The New England Journal of Medicine
|October 11, 2002
Summary
Patients with atopic dermatitis have lower levels of skin antimicrobial peptides cathelicidins (LL-37) and beta-defensins (HBD-2). This deficiency may explain their increased susceptibility to Staphylococcus aureus infections.
Area of Science:
- Dermatology
- Immunology
- Microbiology
Background:
- Human skin's innate immune system relies on antimicrobial peptides like cathelicidins (LL-37) and beta-defensins.
- These peptides are typically low in normal skin but increase in inflammatory conditions like psoriasis.
- Expression levels of LL-37 and human beta-defensin 2 (HBD-2) were compared in inflamed skin from atopic dermatitis and psoriasis patients.
Purpose of the Study:
- To quantify and compare the expression of LL-37 and HBD-2 in skin affected by atopic dermatitis versus psoriasis.
- To investigate the antimicrobial activity of these peptides against Staphylococcus aureus.
Main Methods:
- Immunohistochemical analysis of skin biopsy specimens to detect LL-37 and HBD-2 protein.
- Immunodot blot and Western blot analyses to quantify peptide levels.
- Quantitative real-time RT-PCR to measure LL-37 and HBD-2 mRNA expression.
- Colony-forming assays to assess antimicrobial activity against Staphylococcus aureus.
Main Results:
- Psoriatic skin showed abundant LL-37 and HBD-2, while atopic dermatitis lesions had significantly decreased levels of both peptides.
- RT-PCR confirmed significantly lower LL-37 and HBD-2 mRNA expression in atopic dermatitis compared to psoriasis.
- Combined LL-37 and HBD-2 demonstrated synergistic antimicrobial activity against Staphylococcus aureus.
Conclusions:
- Reduced expression of antimicrobial peptides (LL-37 and HBD-2) in atopic dermatitis may underlie the increased susceptibility to Staphylococcus aureus skin infections.
- Understanding these deficiencies could inform future therapeutic strategies for atopic dermatitis.
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