ArticleThe Journal of allergy and clinical immunology2019
Injury, dysbiosis, and filaggrin deficiency drive skin inflammation through keratinocyte IL-1α release.
Article in The Journal of allergy and clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 77 citations in OpenAlex.
- Eczema-like Granular Parakeratosis Exhibits Inflammatory Keratinocyte Remodeling and Aberrant Epidermal Differentiation.International journal of molecular sciences · 2026Article
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- Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- A λ-Carrageenan-Enriched Sulfated Galactan fromMarine drugs · 2026Article
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- An in silico approach deciphering the commensal dynamics in the cutaneous milieu.NPJ systems biology and applications · 2025Article
- The stratum corneum barrier: impaired function in relation to associated lipids and proteins.Tissue barriers · 2025Review
- The Central Roles of Keratinocytes in Coordinating Skin Immunity.The Journal of investigative dermatology · 2024Review
- Light-emitting diode irradiation at 590 nm combined with active substances modulates ultraviolet B radiation-induced keratinocyte inflammation.Lasers in medical science · 2024Article
- Diabetic Wound Keratinocytes Induce Macrophage JMJD3-Mediated Nlrp3 Expression via IL-1R Signaling.Diabetes · 2024Article
- Maternal influences on offspring food allergy.Immunological reviews · 2024Review
- TLR9 activation in large wound induces tissue repair and hair follicle regeneration via γδT cells.Cell death & disease · 2024Article
- Genetic and Immunological Pathogenesis of Atopic Dermatitis.The Journal of investigative dermatology · 2024Review
- Adding Fuel to the Fire? The Skin Microbiome in Atopic Dermatitis.The Journal of investigative dermatology · 2024Review
- The epithelium takes the stage in asthma and inflammatory bowel diseases.Frontiers in cell and developmental biology · 2024Review
- The causal effects of inflammatory and autoimmune skin diseases on thyroid diseases: evidence from Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Crisaborole efficacy in murine models of skin inflammation and Staphylococcus aureus infection.Experimental dermatology · 2023Article
- Apigenin: A Therapeutic Agent for Treatment of Skin Inflammatory Diseases and Cancer.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
23 authors at 8 institutions in 3 countries.
Funding
Abstract
backgroundAtopic dermatitis (AD) is associated with epidermal barrier defects, dysbiosis, and skin injury caused by scratching. In particular, the barrier-defective epidermis in patients with AD with loss-of-function filaggrin mutations has increased IL-1α and IL-1β levels, but the mechanisms by which IL-1α, IL-1β, or both are induced and whether they contribute to the aberrant skin inflammation in patients with AD is unknown.
objectiveWe sought to determine the mechanisms through which skin injury, dysbiosis, and increased epidermal IL-1α and IL-1β levels contribute to development of skin inflammation in a mouse model of injury-induced skin inflammation in filaggrin-deficient mice without the matted mutation (ft/ft mice).
methodsSkin injury of wild-type, ft/ft, and myeloid differentiation primary response gene-88-deficient ft/ft mice was performed, and ensuing skin inflammation was evaluated by using digital photography, histologic analysis, and flow cytometry. IL-1α and IL-1β protein expression was measured by means of ELISA and visualized by using immunofluorescence and immunoelectron microscopy. Composition of the skin microbiome was determined by using 16S rDNA sequencing.
resultsSkin injury of ft/ft mice induced chronic skin inflammation involving dysbiosis-driven intracellular IL-1α release from keratinocytes. IL-1α was necessary and sufficient for skin inflammation in vivo and secreted from keratinocytes by various stimuli in vitro. Topical antibiotics or cohousing of ft/ft mice with unaffected wild-type mice to alter or intermix skin microbiota, respectively, resolved the skin inflammation and restored keratinocyte intracellular IL-1α localization.
conclusionsTaken together, skin injury, dysbiosis, and filaggrin deficiency triggered keratinocyte intracellular IL-1α release that was sufficient to drive chronic skin inflammation, which has implications for AD pathogenesis and potential therapeutic targets.
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