ArticleThe Journal of allergy and clinical immunology2015
Filaggrin breakdown products determine corneocyte conformation in patients with atopic dermatitis.
Article in The Journal of allergy and clinical immunology, 2015. 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, 119 citations in OpenAlex.
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- Exome-wide evidence of compound heterozygous effects across common phenotypes in the UK Biobank.Cell genomics · 2024Article
- Efficacy of Topical Application of a Skin Moisturizer Containing Pseudo-Ceramide and a Eucalyptus Leaf Extract on Atopic Dermatitis: A Review.Journal of clinical medicine · 2024Review
- Moderate to severe atopic dermatitis in children: focus on systemic Th2 cytokine receptor antagonists and Janus kinase inhibitors.Clinical and experimental pediatrics · 2024Article
- Stratum corneum nanotexture feature detection using deep learning and spatial analysis: a noninvasive tool for skin barrier assessment.GigaScience · 2024Article
- Understanding the role ofFrontiers in medicine · 2024Review
- Effect of altered human exposome on the skin and mucosal epithelial barrier integrity.Tissue barriers · 2023Article
- Macroscopic Skin Examination Can Determine the Number of Strips Necessary to Study theVeterinary sciences · 2023Article
- Exome-wide evidence of compound heterozygous effects across common phenotypes in the UK Biobank.medRxiv : the preprint server for health sciences · 2023Article
- The A domain of clonal complex 1-type fibronectin binding protein B promotes adherence and biofilm formation inMicrobiology (Reading, England) · 2023Article
- Circadian Oscillations in Skin and Their Interconnection with the Cycle of Life.International journal of molecular sciences · 2023Review
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- Microbial derived antimicrobial peptides as potential therapeutics in atopic dermatitis.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundLoss-of-function (LOF) mutations in the filaggrin gene (FLG) are a well-replicated risk factor for atopic dermatitis (AD) and are known to cause an epidermal barrier defect. The nature of this barrier defect is not fully understood. Patients with AD with FLG LOF mutations are known to have more persistent disease, more severe disease, and greater risk of food allergies and eczema herpeticum. Abnormalities in corneocyte morphology have been observed in patients with AD, including prominent villus-like projections (VP); however, these ultrastructural features have not been systematically studied in patients with AD in relation to FLG genotype and acute and convalescent status.
objectiveWe sought to quantitatively explore the relationship between FLG genotype, filaggrin breakdown products (natural moisturizing factor [NMF]), and corneocyte morphology in patients with AD.
methodsWe studied 15 children at first presentation of AD and after 6 weeks of standard therapy. We applied atomic force microscopy to study corneocyte conformation in patients with AD stratified by FLG status and NMF level. By using a new quantitative methodology, the number of VPs per investigated corneocyte area was assessed and expressed as the Dermal Texture Index score. Corneocytes were also labeled with an anti-corneodesmosin antibody and visualized with scanning electron microscopy.
resultsWe found a strong correlation between NMF levels and Dermal Texture Index scores in both acute and convalescent states (respective r = -0.80 and -0.75, P < .001 and P = .002). Most, but not all, VPs showed the presence of corneodesmosin abundantly all over the cell surface in homozygous/compound heterozygous FLG patients and, to a lesser extent, in heterozygous and wild-type patients.
conclusionsNMF levels are highly correlated with corneocyte morphology in patients with AD. These corneocyte conformational changes shed further insight into the filaggrin-deficient phenotype and help explain the barrier defect in patients with AD with FLG LOF mutations.
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