Mechanism of HBD-3 deficiency in atopic dermatitis |
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Authors: | Howell Michael D Boguniewicz Mark Pastore Saveria Novak Natalija Bieber Thomas Girolomoni Giampiero Leung Donald Y M |
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Institution: | Division of Allergy and Immunology, Department of Pediatrics, The National Jewish Medical and Research Center, Room K926, 1400 Jackson Street, Denver, CO 80206, USA. |
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Abstract: | Extrinsic atopic dermatitis (EAD) and intrinsic atopic dermatitis (IAD) patients suffer from recurrent bacterial and viral infections. In this study, we demonstrate significantly decreased expression of human beta defensin (HBD)-3, a potent antimicrobial peptide (AMP), in lesional skin of both IAD (p<0.01) and EAD patients (p<0.01), as compared to psoriasis patients. Using primary keratinocytes from EAD and IAD patients, we determined that the deficiency in HBD-3 expression is an acquired rather than a constitutive defect. Furthermore, we demonstrate the down-regulatory effect of IL-4, IL-10, and IL-13 - which are over-expressed in the skin of AD patients - on HBD-3 expression in keratinocytes. Additionally, treatment of EAD skin explants with antibodies against IL-4, IL-10, and IL-13 augmented the expression of HBD-3. These studies suggest that neutralizing the Th2 cytokine milieu in AD skin may augment the innate immune response against bacterial and viral pathogens. |
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Keywords: | Antimicrobial peptides Cytokines Extrinsic atopic dermatitis Intrinsic atopic dermatitis |
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