Trial reportThe Journal of allergy and clinical immunology2025
CERS1 is a biomarker of Staphylococcus aureus abundance and atopic dermatitis severity.
Trial report in The Journal of allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03389893 (Effect of Dupilumab), which is not on this map. Cited by 6 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Effect of Dupilumab (Anti-IL4Rα) on the Host-Microbe Interface in Atopic Dermatitis, Dupilumab Study
Who cites it
6 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Novel Therapeutic Strategies for Atopic Dermatitis: Biomarker Modulation and Clinical Implications. A Systematic Review.Clinical reviews in allergy & immunology · 2026Pooled it
- Current insights and trends in atopic dermatitis and microbiota interactions: a systematic review and bibliometric analysis.Frontiers in microbiology · 2025Pooled it
- Endogenous Ceramide 24:1 Constrains Th17-Driven Neutrophilic Inflammation by Antagonizing EP2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microbiota-directed therapies for atopic dermatitis: a three-tier framework for inflammation control, immune modulation, and microbiome restoration.Frontiers in immunology · 2026Review
- Symbiotic bacteria-mediated imbalance and repair of immune homeostasis: exploring novel mechanisms of microbiome-host interactions in atopic dermatitis.Frontiers in immunology · 2025Review
- Skin Barrier Repair and Nursing Care in Patients with Atopic Dermatitis: A Narrative Review.International journal of general medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
backgroundAtopic dermatitis (AD) is an inflammatory skin condition characterized by widely variable cutaneous Staphylococcus aureus abundance that contributes to disease severity and rapidly responds to type 2 immune blockade (ie, dupilumab). The molecular mechanisms regulating S aureus levels between AD subjects remain poorly understood.
objectiveWe investigated host genes that may be predictive of S aureus abundance and correspond with AD severity.
methodsWe studied data derived from the National Institutes of Health/National Institute of Allergy and Infectious Diseases-funded (NCT03389893 [ADRN-09]) randomized, double-blind, placebo-controlled multicenter study of dupilumab in adults (n = 71 subjects) with moderate-to-severe AD. Bulk RNA sequencing of skin biopsy samples (n = 57 lesional, 55 nonlesional) was compared to epidermal S aureus abundance, lipidomic, and AD clinical measures.
resultsS aureus abundance and ceramide synthase 1 (CERS1) expression positively correlated at baseline across both nonlesional (r = 0.29, P = .030) and lesional (r = 0.41, P = .0015) skin. Lesional CERS1 expression also positively correlated with AD severity (ie, SCORAD r = 0.44, P = .0006) and skin barrier dysfunction (transepidermal water loss area under the curve r = 0.31, P = .025) at baseline. CERS1 expression (forms C
conclusionCERS1 is a unique molecular biomarker of S aureus abundance and AD severity that may contribute to dysfunctional skin barrier and shorter-chain sphingolipid composition through fatty acid sequestration as a maladaptive compensatory response to reduced ELOVL6.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.