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In vivo quantitative analysis of advanced glycation end products in atopic dermatitis—Possible culprit for the comorbidities?
Author(s) -
Hong Ji Yeon,
Kim Min Jeong,
Hong Jun Ki,
Noh Hyun Ha,
Park Kui Young,
Lee Mi Kyung,
Seo Seong Jun
Publication year - 2020
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.14167
Subject(s) - glycation , rage (emotion) , atopic dermatitis , medicine , receptor , culprit , inflammation , advanced glycation end product , corneocyte , immunology , endocrinology , pathology , biology , stratum corneum , neuroscience , myocardial infarction
Advanced glycation end products (AGEs) interact with the membrane‐bound receptor for AGEs (RAGE), consequently amplifying the inflammatory response. Soluble receptor for AGE (sRAGE) and endogenous secretory RAGE (esRAGE) act as decoys for AGE and competitively sequester RAGE ligands, thereby serving a cytoprotective role. Our objective was to investigate AGE expression and their receptors in the serum and skin of patients with atopic dermatitis (AD). In this case‐control study, the levels of AGE, sRAGE and esRAGE were measured in the blood samples and corneocytes of 29 adult patients with AD and 12 healthy controls by ELISA. Corneocyte AGE levels increased in the AD group ( P = .002). Higher corneocyte AGE levels were observed in the severe AD than in the milder form of AD. No significant difference in serum AGE level was observed in patients with AD and healthy controls. Serum sRAGE markedly decreased in patients with AD ( P = .007) and serum esRAGE followed a similar trend. In conclusion, dermal accumulation of AGE in AD may have a role in fuelling skin inflammation. The potential after‐effects of reduced neutralizer on systemic risk need further evaluation.