Profile of skin barrier proteins (filaggrin, claudins 1 and 4) and Th1/Th2/Th17 cytokines in adults with atopic dermatitis
Journal of the European Academy of Dermatology and Venereology, 2015•Wiley Online Library
Background Atopic dermatitis (AD) in adults and profile of skin barrier proteins and
inflammatory cytokines. Objective Evaluation of the expression of skin barrier proteins such
as filaggrin, claudins 1 and 4 and of circulating inflammatory cytokines (Th1/Th2/Th17) in
adults with AD. Methods Thirty‐three adult patients with AD diagnosed according to the
Hanifin & Rajkacriteria, and 25 healthy controls were enrolled in the study. AD severity was
measured by Eczema Area and Severity Index (EASI). Laboratory assays included …
inflammatory cytokines. Objective Evaluation of the expression of skin barrier proteins such
as filaggrin, claudins 1 and 4 and of circulating inflammatory cytokines (Th1/Th2/Th17) in
adults with AD. Methods Thirty‐three adult patients with AD diagnosed according to the
Hanifin & Rajkacriteria, and 25 healthy controls were enrolled in the study. AD severity was
measured by Eczema Area and Severity Index (EASI). Laboratory assays included …
Background
Atopic dermatitis (AD) in adults and profile of skin barrier proteins and inflammatory cytokines.
Objective
Evaluation of the expression of skin barrier proteins such as filaggrin, claudins 1 and 4 and of circulating inflammatory cytokines (Th1/Th2/Th17) in adults with AD.
Methods
Thirty‐three adult patients with AD diagnosed according to the Hanifin & Rajkacriteria, and 25 healthy controls were enrolled in the study. AD severity was measured by Eczema Area and Severity Index (EASI). Laboratory assays included immunohistochemistry analysis of skin barrier proteins, such as filaggrin, claudins 1 and 4 and interleukin‐17 (IL‐17) from skin samples and determination of circulating cytokine levels (IL‐2, 4, 5, 6, 10, 17A, TNF and IFN‐γ) by flow cytometry (Cytometric Bead Array).
Results
We observed a reduced expression of filaggrin and claudin 1 in lesional skin of AD patients, when compared to controls. There was an inverse correlation of filaggrin expression and disease severity. In addition, IL‐17 expression was enhanced in AD patients. Similarly, higher levels of inflammatory cytokines (IL‐2, 5, 6, 10, 17A and IFN‐γ) were found in AD patients.
Conclusion
Our data reinforce the role of an altered skin barrier in the pathogenesis of AD. Our results show not only reduced expression of filaggrin and claudin 1 in lesional atopic skin but also inverse correlation of filaggrin expression and disease severity. Moreover, elevation of in situ IL‐17 and of circulating interleukin levels in AD emphasize the systemic, inflammatory profile of this defective skin barrier dermatosis.
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