Interleukin-10 Downregulates Anti-Microbial Peptide Expression in Atopic Dermatitis

Recurrent skin infections in extrinsic atopic dermatitis (EAD) may be because of the suppression of anti-microbial peptide (AMP) expression by interleukin (IL)-4 and IL-13. Twenty to thirty percent of AD, however, are classified as intrinsic atopic dermatitis (IAD). They exhibit normal serum IgE lev...

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Veröffentlicht in:Journal of investigative dermatology 2005-10, Vol.125 (4), p.738-745
Hauptverfasser: Howell, Michael D., Novak, Natalija, Bieber, Thomas, Pastore, Saveria, Girolomoni, Giampiero, Boguniewicz, Mark, Streib, Joanne, Wong, Cathy, Gallo, Richard L., Leung, Donald Y.M.
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Sprache:eng
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Zusammenfassung:Recurrent skin infections in extrinsic atopic dermatitis (EAD) may be because of the suppression of anti-microbial peptide (AMP) expression by interleukin (IL)-4 and IL-13. Twenty to thirty percent of AD, however, are classified as intrinsic atopic dermatitis (IAD). They exhibit normal serum IgE levels, no allergen-specific sensitization, and lower levels of IL-4 and IL-13 than EAD. Both forms of AD have increased propensity to skin infection, suggesting a novel mechanism for infection in IAD. In this study, we observed significantly decreased human β-defensin (HBD)-2 gene expression in the skin of both IAD (p=0.010) and EAD (p=0.004), as compared with psoriasis patients. Conversely, IAD (p=0.019) and EAD (p=0.002) skin lesions exhibited elevated IL-10 gene expression when compared with psoriasis. Using primary keratinocytes, we found that the deficiency in AMP expression is an acquired rather than a constitutive defect. Interestingly, neutralizing antibodies to IL-10 augmented the production of tumor necrosis factor-α and interferon-γ by peripheral blood mononuclear cell from AD patients. Additionally, treatment of AD skin explants with anti-IL-10 augmented the expression of both HBD-2 and LL-37. Thus, increased levels of IL-10 may contribute to the AMP deficiency in both IAD and EAD by reducing cytokines that induce AMP.
ISSN:0022-202X
1523-1747
DOI:10.1111/j.0022-202X.2005.23776.x