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Air Pollution and Atopic Dermatitis (AD): The Impact of Particulate Matter (PM10) on an AD Mouse-Model.
Woo, Yu Ri; Park, Seo-Yeon; Choi, Keonwoo; Hong, Eun Sun; Kim, Sungjoo; Kim, Hei Sung.
Afiliação
  • Woo YR; Department of Dermatology, Incheon St. Mary's Hospital, The Catholic University of Korea, Seoul 06591, Korea.
  • Park SY; Department of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul 06591, Korea.
  • Choi K; Department of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul 06591, Korea.
  • Hong ES; Department of Dermatology, Incheon St. Mary's Hospital, The Catholic University of Korea, Seoul 06591, Korea.
  • Kim S; Department of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul 06591, Korea.
  • Kim HS; Department of Dermatology, Incheon St. Mary's Hospital, The Catholic University of Korea, Seoul 06591, Korea.
Int J Mol Sci ; 21(17)2020 Aug 24.
Article em En | MEDLINE | ID: mdl-32846909
ABSTRACT
Air pollution reportedly contributes to the development and exacerbation of atopic dermatitis (AD). However, the exact mechanism underlying this remains unclear. To examine the relationship between air pollution and AD, a clinical, histological, and genetic analysis was performed on particulate matter (PM)-exposed mice. Five-week-old BALB/c mice were randomly divided into four groups (control group, ovalbumin (OVA) group, PM group, OVA + PM group; n = 6) and treated with OVA or PM10, alone or together. Cutaneous exposure to OVA and PM10 alone resulted in a significant increase in skin severity scores, trans-epidermal water loss (TEWL) and epidermal thickness compared to the control group at Week 6. The findings were further accentuated in the OVA + PM group showing statistical significance over the OVA group. A total of 635, 501, and 2149 genes were found to be differentially expressed following OVA, PM10, and OVA + PM10 exposure, respectively. Strongly upregulated genes included RNASE2A, S100A9, SPRR2D, THRSP, SPRR2A1 (OVA vs. control), SPRR2D, S100A9, STFA3, CHIL1, DBP, IL1B (PM vs. control) and S100A9, SPRR2D, SPRR2B, S100A8, SPRR2A3 (OVA + PM vs. control). In comparing the groups OVA + PM with OVA, 818 genes were differentially expressed with S100A9, SPRR2B, SAA3, S100A8, SPRR2D being the most highly upregulated in the OVA + PM group. Taken together, our study demonstrates that PM10 exposure induces/aggravates skin inflammation via the differential expression of genes controlling skin barrier integrity and immune response. We provide evidence on the importance of public awareness in PM-associated skin inflammation. Vigilant attention should be paid to all individuals, especially to those with AD.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Pele / Dermatite Atópica / Poluição do Ar / Material Particulado Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Pele / Dermatite Atópica / Poluição do Ar / Material Particulado Idioma: En Ano de publicação: 2020 Tipo de documento: Article