title: DAMP molecules S100A9 and S100A8 activated by IL-17A and house-dust mites are increased in atopic dermatitis.
abstract: S100A9 and S100A8 are called damage-associated molecular pattern (DAMP) molecules because of their pro-inflammatory properties. Few studies have evaluated S100A9 and S100A8 function as DAMP molecules in atopic dermatitis (AD). We investigated how house-dust mites affect S100A9 and S100A8 expression in Th2 cytokine- and Th17 cytokine-treated keratinocytes, and how secretion of these molecules affects keratinocyte-derived cytokines. Finally, we evaluated expression of these DAMP molecules in AD patients. S100A9 expression and S100A8 expression were strongly induced in IL-17A- and Dermatophagoides (D.) farinae-treated keratinocytes, respectively. Furthermore, co-treatment with D. farinae and IL-17A strongly increased expression of S100A9 and S100A8 compared with D. farinae-Th2 cytokine co-treatment. The IL-33 mRNA level increased in a dose-dependent manner in S100A9-treated keratinocytes, but TSLP expression did not change. S100A8/A9 levels were also higher in the lesional skin and serum of AD patients, and correlated with disease severity. Taken together, S100A9 and S100A8 may be involved in inducing DAMP-mediated inflammation in AD triggered by IL-17A and house-dust mites.
authors.affiliation: Department of Dermatology & Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea; Department of Dermatology, Yanbian University Hospital, Yanji, Jilin, China.
authors.forename: Shan
authors.initials: S
authors.lastname: Jin
authors.forename: Chang Ook
authors.initials: CO
authors.lastname: Park
authors.forename: Jung U
authors.initials: JU
authors.lastname: Shin
authors.forename: Ji Yeon
authors.initials: JY
authors.lastname: Noh
authors.forename: Yun Sun
authors.initials: YS
authors.lastname: Lee
authors.forename: Na Ra
authors.initials: NR
authors.lastname: Lee
authors.forename: Hye Ran
authors.initials: HR
authors.lastname: Kim
authors.forename: Seongmin
authors.initials: S
authors.lastname: Noh
authors.forename: Young
authors.initials: Y
authors.lastname: Lee
authors.forename: Jeung-Hoon
authors.initials: JH
authors.lastname: Lee
authors.forename: Kwang Hoon
authors.initials: KH
authors.lastname: Lee
mesh_terms: D000818:Animals; D040501:Calgranulin A / Q000378:metabolism*; D040502:Calgranulin B / Q000378:metabolism*; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D040001:Dermatophagoides farinae / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D007113:Immunity, Innate; D020381:Interleukin-17 / Q000378:metabolism*; D000067596:Interleukin-33; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics; D015603:Keratinocytes / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D015854:Up-Regulation
chemical_list: D040501:Calgranulin A; D040502:Calgranulin B; D016207:Cytokines; C508717:IL17A protein, human; C506536:IL33 protein, human; D020381:Interleukin-17; D000067596:Interleukin-33; D007378:Interleukins; D012333:RNA, Messenger
keywords: Dermatophagoides farinae; IL-17A; IL-33; S100A8; S100A9; atopic dermatitis