ArticleArchives of dermatological research2024
Cutaneous inflammasome driving ASC / gasdermin-D activation and IL-1β-secreting macrophages in severe atopic dermatitis.
Article in Archives of dermatological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Structural Characterization of Squid Peptides and Evaluation of Their Antiphotoaging Activity in Nude Mice.Preventive nutrition and food science · 2026Article
- Translational insights into interleukin-driven macrophage polarization as diagnostic biomarkers for atopic dermatitis-a narrative review.Frontiers in molecular biosciences · 2026Review
- Therapeutic Potential of Isoniazid in Inflammatory Skin Diseases: A Review.Clinical, cosmetic and investigational dermatology · 2026Review
- Regulated Cell Death Pathways in Chondrocytes During Septic Arthritis: Current Evidence and Future Perspectives.Journal of inflammation research · 2026Review
- IL-33-primed NLRP3 inflammasome in basophils drives IL-1β production and initiates atopic dermatitis inflammation.Cell death discovery · 2025Article
- Pathogenesis of Inflammation in Skin Disease: From Molecular Mechanisms to Pathology.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Atopic dermatitis (AD) is an inflammatory skin disease with intense pruritus, and chronic skin colonization by Staphylococcus aureus. To understand the inflammatory status in AD, we investigated the inflammasome complex, that activates ASC (Apoptosis-associated speck-like protein containing a CARD), caspase-1 and GSDMD (gasdermin-D), and production of IL-1β and IL-18. We aimed to evaluate the expression of the inflammasome pathway in the skin of adults with AD. Thirty patients with moderate to severe AD and 20 healthy controls were enrolled in the study. We performed the analysis of the inflammasome components NLRP1, NLRP3, AIM-2, IL-1β, IL-18, Caspase-1, ASC, GSDMD, and CD68 expression (macrophage marker) by immunohistochemistry and immunofluorescence. The main findings included increased expression of NLRP3, NLRP1 and AIM-2 at dermal level of severe AD; augmented IL-18 and IL-1β expression at epidermis of moderate and severe patients, and in the dermis of severe AD; augmented expression of ASC, caspase-1 and GSDMD in both epidermis and dermis of moderate and severe AD. We detected positive correlation between caspase-1, GSDMD and IL-1β (epidermis) and caspase-1 (dermis) and AD severity; NLRP3, AIM-2 and IL-1β, and NLRP3 with IL-18 in the epidermis; ASC, GSDMD and IL-1β, and NLRP3, AIM-2, caspase-1, and IL-18 in the dermis. We also evidenced the presence of CD68
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Registered trials
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