Interleukin-10 Downregulates Anti-Microbial Peptide Expression in Atopic Dermatitis
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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 beta-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-alpha and interferon-gamma 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.
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AMP expression is highly dependent on the cytokine milieu present in the skin and proinflammatory cytokines such as IL-1, IL-6, IL-8, and TNFα are typically strong inducers of AMPs, whereas IL-4, IL-13, and IL-10 have been shown to dampen AMP responses.
“AMP expression is highly dependent on the cytokine milieu present in the skin and proinflammatory cytokines, such as IL-1, IL-6, IL-8, and tumor necrosis factor α (TNFα), are typically strong inducers of AMPs, whereas IL-4, IL-13, and IL-10 have been shown to dampen AMP responses.33–35”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [35]
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Self-citation
- Authors
- Howell, M. D., Novak, N., Bieber, T., Pastore, S., Girolomoni, G., Boguniewicz, M., Streib, J., Wong, C., Gallo, R. L., & Leung, D. Y. M.
- Affiliations
- National Jewish Health (US)
- University of Bonn (DE)
- Istituto Dermopatico dell'Immacolata (IT)
- University of California San Diego (US)
- Corresponding author
- Leung, Donald Y.M.
- ORCID
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2005-10
- Volume
- 125
- Issue
- 4
- Pages
- 738-745
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2092527023
- Cited by
- 193
- References
- 34
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 4 · 2022: 7 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 8 · 2017: 10 · 2016: 3 · 2015: 9 · 2014: 10 · 2013: 13 · 2012: 9
- FWCI
- 22.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (454/1-1, 454/2-1)
- National Institutes of Health (T32 AI 07365)
- Ministero della Salute (AI052453, HL37260, HL36577, R21 AR051634-01, AR45676, AR41256)
- Cancer Center, University of Colorado
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Keywords
- IL-10, atopic dermatitis, antimicrobial peptides, human beta-defensin 2, LL-37, skin infections, intrinsic atopic dermatitis, extrinsic atopic dermatitis, keratinocytes, IL-4, IL-13, TNF-α, interferon-gamma, psoriasis
- MeSH terms
- Adult, Cells, Cultured, Dermatitis, Atopic, Gene Expression Regulation, Humans, Immunohistochemistry, Middle Aged, Psoriasis, Down-Regulation, Interleukin-10, Interleukin-13, beta-Defensins, Antimicrobial Cationic Peptides, Cathelicidins
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