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


Journal

The British journal of dermatology
ISSN: 1365-2133
Titre abrégé: Br J Dermatol
Pays: England
ID NLM: 0004041

Informations de publication

Date de publication:
03 2019
Historique:
accepted: 18 07 2018
pubmed: 23 8 2018
medline: 25 2 2020
entrez: 23 8 2018
Statut: ppublish

Résumé

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. 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. 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. 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). 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.

Sections du résumé

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.

Identifiants

pubmed: 30132823
doi: 10.1111/bjd.17088
pmc: PMC6446820
doi:

Substances chimiques

Biomarkers 0
Chemokines 0
Cytokines 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

586-596

Subventions

Organisme : National Centre for the Replacement, Refinement and Reduction of Animals in Research
ID : NC/P00217X/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 092530/Z/10/Z
Pays : United Kingdom
Organisme : Wellcome Trust Strategic Award
ID : 098439/Z/12/Z
Pays : International
Organisme : Wellcome Trust
ID : 090066/B/09/Z
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2018 The Authors. British Journal of Dermatology published by John Wiley & Sons Ltd on behalf of British Association of Dermatologists.

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Auteurs

M A McAleer (MA)

National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.
Paediatric Dermatology, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.

I Jakasa (I)

Laboratory for Analytical Chemistry, Department of Chemistry and Biochemistry, Faculty of Food Technology and Biotechnology, University of Zagreb, Zagreb, Croatia.

G Hurault (G)

Department of Bioengineering, Imperial College London, London, U.K.

P Sarvari (P)

Department of Bioengineering, Imperial College London, London, U.K.

W H I McLean (WHI)

Dermatology and Genetic Medicine, University of Dundee, Dundee, U.K.

R J Tanaka (RJ)

Department of Bioengineering, Imperial College London, London, U.K.

S Kezic (S)

Amsterdam UMC, University of Amsterdam, Coronel Institute of Occupational Health, Amsterdam Public Health research institute, Meibergdreef 9, Amsterdam, the Netherlands.

A D Irvine (AD)

National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.
Paediatric Dermatology, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.
Clinical Medicine, Trinity College Dublin, Dublin, Ireland.

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