Increased serum levels of interleukin 33 in patients with atopic dermatitis
Background Interleukin (IL)-33 is a new member of the IL-1 cytokine family and a promoter of T helper type 2 (Th2) inflammation. IL-33 may be involved in the pathogenesis of atopic dermatitis (AD), but its relationship with disease severity, laboratory markers, and eruption types in patients with AD...
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Published in | Journal of the American Academy of Dermatology Vol. 70; no. 5; pp. 882 - 888 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.05.2014
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Subjects | |
Online Access | Get full text |
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Summary: | Background Interleukin (IL)-33 is a new member of the IL-1 cytokine family and a promoter of T helper type 2 (Th2) inflammation. IL-33 may be involved in the pathogenesis of atopic dermatitis (AD), but its relationship with disease severity, laboratory markers, and eruption types in patients with AD are unclear. Objective The aim of this study was to quantify serum IL-33 levels in patients with AD and to examine relationships with disease severity, laboratory markers, and eruption types. Methods Serum IL-33 was measured by enzyme-linked immunosorbent assay in patients with AD, chronic idiopathic urticaria, and psoriasis and in healthy control subjects. Results Serum levels of IL-33 were significantly higher in patients with AD compared with those in patients with urticaria and psoriasis and in healthy control subjects, and were correlated with the disease severity of AD. IL-33 levels were also significantly correlated with excoriation and xerosis scores, but not with blood eosinophilia, serum IgE, serum thymus and activation-related chemokine, and serum lactate dehydrogenase. Elevated IL-33 levels were significantly reduced after improvement of skin lesions by drug treatment. Limitation A limitation in the study was the small number of subjects. Conclusion Our results suggest that IL-33 released from mechanically injured or barrier-disrupted skin may increase inflammation in AD. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0190-9622 1097-6787 |
DOI: | 10.1016/j.jaad.2014.01.867 |