Bilirubin oxidation derived from oxidative stress is associated with disease severity of atopic dermatitis in adults
Author(s) -
Shibama S.,
Ugajin T.,
Yamaguchi T.,
Yokozeki H.
Publication year - 2019
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/ced.13674
Subject(s) - atopic dermatitis , oxidative stress , bilirubin , medicine , urinary system , pathogenesis , immunology , gastroenterology , pathology
Summary Background Bilirubin is an essential antioxidant. Its oxidative metabolites, biopyrrins, are sensitive urinary markers of oxidative stress. Multiple studies suggest that oxidative stress affects the pathogenesis of skin diseases such as atopic dermatitis ( AD ). Aim To examine oxidative stress‐induced bilirubin oxidation and its association with AD pathogenesis in adults. Methods In total, 11 patients with AD and 7 healthy controls ( HC s) were enrolled. Bilirubin oxidation profiles in the combined urine of the patients and that of the HC s were examined using high‐performance liquid chromatography ( HPLC ) and fast atom bombardment mass spectrometry. The concentrations of urinary biopyrrins and serum biomarkers for AD disease severity, such as IgE and thymus and activation‐regulated chemokine ( TARC )/ CCL 17, were measured by ELISA to determine correlations between urinary biopyrrins and serum biomarkers. Local bilirubin oxidation in AD skin lesions was assessed by immunohistochemical analyses using two antibodies against bilirubin. Results Levels of dipyrrole‐monopyrrole‐aldehyde, a novel urinary biopyrrin, were higher in patients with AD than in HC s, and increased with disease severity based on the SCOR ing Atopic Dermatitis ( SCORAD ) objective scoring system. Additionally, urinary biopyrrin levels correlated significantly with serum IgE and TARC / CCL 17 levels. Furthermore, immunohistochemical analyses revealed that biopyrrins were strongly expressed in both infiltrating and resident cells in AD lesions. However, bilirubin was expressed at low levels in the lesions, suggesting that bilirubin oxidation is augmented in AD lesions. Conclusions Bilirubin oxidation derived from oxidative stress in the skin lesions can be associated with disease severity of AD .