摘要
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.
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 lAD. 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, lAD （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,
