Risa Tamagawa-Mineoka1, Yasutaro Okuzawa2, Koji Masuda2, Norito Katoh2. 1. Department of Dermatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. Electronic address: risat@koto.kpu-m.ac.jp. 2. Department of Dermatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Abstract
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.
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.
Authors: Sean J Lund; Alex Portillo; Kellen Cavagnero; Rachel E Baum; Luay H Naji; Jana H Badrani; Amit Mehta; Michael Croft; David H Broide; Taylor A Doherty Journal: J Immunol Date: 2017-06-30 Impact factor: 5.422
Authors: Karina P Debes; Nathalie A Evdina; Ann Laigaard; Julie M Larsen; Line F Zachariassen; Camilla H F Hansen; Axel K Hansen Journal: Comp Med Date: 2019-11-19 Impact factor: 0.982