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Systemic and stratum corneum biomarkers of severity in infant atopic dermatitis include markers of innate and T helper cell‐related immunity and angiogenesis

BACKGROUND: Biomarkers of atopic dermatitis (AD) are largely lacking, especially in infant AD. Those that have been examined to date have focused mostly on serum cytokines, with few on noninvasive biomarkers in the skin. OBJECTIVES: We aimed to explore biomarkers obtainable from noninvasive sampling...

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Detalles Bibliográficos
Autores principales: McAleer, M.A., Jakasa, I., Hurault, G., Sarvari, P., McLean, W.H.I., Tanaka, R.J., Kezic, S., Irvine, A.D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446820/
https://www.ncbi.nlm.nih.gov/pubmed/30132823
http://dx.doi.org/10.1111/bjd.17088
Descripción
Sumario:BACKGROUND: Biomarkers of atopic dermatitis (AD) are largely lacking, especially in infant AD. Those that have been examined to date have focused mostly on serum cytokines, with few on noninvasive biomarkers in the skin. OBJECTIVES: We aimed to explore biomarkers obtainable from noninvasive sampling of infant skin. We compared these with plasma biomarkers and structural and functional measures of the skin barrier. METHODS: We recruited 100 infants at first presentation with AD, who were treatment naive to topical or systemic anti‐inflammatory therapies, and 20 healthy children. We sampled clinically unaffected skin by tape stripping the stratum corneum (SC). Multiple cytokines and chemokines and natural moisturizing factor were measured in the SC and plasma. We recorded disease severity and skin barrier function. RESULTS: Nineteen SC and 12 plasma biomarkers showed significant differences between healthy and AD skin. Some biomarkers were common to both the SC and plasma, and others were compartment specific. Identified biomarkers of AD severity included T helper 2‐skewed markers [interleukin (IL)‐13, CCL17, CCL22, IL‐5]; markers of innate activation (IL‐18, IL‐1α, IL1β, CXCL8) and angiogenesis (Flt‐1, vascular endothelial growth factor); and others (soluble intercellular adhesion molecule‐1, soluble vascular cell adhesion molecule‐1, IL‐16, IL‐17A). CONCLUSIONS: We identified clinically relevant biomarkers of AD, including novel markers, easily sampled and typed in infants. These markers may provide objective assessment of disease severity and suggest new therapeutic targets, or response measurement targets for AD. Future studies will be required to determine whether these biomarkers, seen in very early AD, can predict disease outcomes or comorbidities.