Interactions between Malassezia and New Therapeutic Agents in Atopic Dermatitis Affecting Skin Barrier and Inflammation in Recombinant Human Epidermis Model
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Y.-J. | - |
dc.contributor.author | Yassa, C. | - |
dc.contributor.author | Park, S.-H. | - |
dc.contributor.author | Song, S.W. | - |
dc.contributor.author | Jung, W.H. | - |
dc.contributor.author | Lee, Y.W. | - |
dc.contributor.author | Kang, H. | - |
dc.contributor.author | Kim, J.-E. | - |
dc.date.accessioned | 2023-10-04T06:40:55Z | - |
dc.date.available | 2023-10-04T06:40:55Z | - |
dc.date.issued | 2023-04 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/67958 | - |
dc.description.abstract | Several studies have reported the pathogenic role of Malassezia in atopic dermatitis (AD); the significance of Malassezia’s influence on AD needs to be further investigated. Dupilumab, a monoclonal antibody to anti-Interleukin (IL) 4Rα, and ruxolitinib, a Janus kinase (JAK)1/2 inhibitor, are the first approved biologics and inhibitors widely used for AD treatment. In this study, we aimed to investigate how Malassezia Restricta (M. restricta) affects the skin barrier and inflammation in AD and interacts with the AD therapeutic agents ruxolitinib and anti-IL4Rα. To induce an in vitro AD model, a reconstructed human epidermis (RHE) was treated with IL-4 and IL-13. M. restricta was inoculated on the surface of RHE, and anti-IL4Rα or ruxolitinib was supplemented to model treated AD lesions. Histological and molecular analyses were performed. Skin barrier and ceramide-related molecules were downregulated by M. restricta and reverted by anti-IL4Rα and ruxolitinib. Antimicrobial peptides, VEGF, Th2-related, and JAK/STAT pathway molecules were upregulated by M. restricta and suppressed by anti-IL4Rα and ruxolitinib. These findings show that M. restricta aggravated skin barrier function and Th2 inflammation and decreased the efficacy of anti-IL4Rα and ruxolitinib. © 2023 by the authors. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | MDPI | - |
dc.title | Interactions between Malassezia and New Therapeutic Agents in Atopic Dermatitis Affecting Skin Barrier and Inflammation in Recombinant Human Epidermis Model | - |
dc.type | Article | - |
dc.identifier.doi | 10.3390/ijms24076171 | - |
dc.identifier.bibliographicCitation | International Journal of Molecular Sciences, v.24, no.7 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000969679900001 | - |
dc.identifier.scopusid | 2-s2.0-85152309186 | - |
dc.citation.number | 7 | - |
dc.citation.title | International Journal of Molecular Sciences | - |
dc.citation.volume | 24 | - |
dc.type.docType | Article | - |
dc.publisher.location | 스위스 | - |
dc.subject.keywordAuthor | anti-IL4Rα | - |
dc.subject.keywordAuthor | atopic dermatitis | - |
dc.subject.keywordAuthor | Malassezia | - |
dc.subject.keywordAuthor | reconstructed human epidermis model | - |
dc.subject.keywordAuthor | ruxolitinib | - |
dc.subject.keywordPlus | PERMEABILITY BARRIER | - |
dc.subject.keywordPlus | ENHANCED EXPRESSION | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | DISEASES | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | CYTOKINES | - |
dc.subject.keywordPlus | DEFENSE | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.