Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques

Abstract Narrow band-ultraviolet B (NB-UVB) is an effective treatment for psoriasis. We aim to generate a potential mechanism of NB-UVB through comparing the transcriptomic profile before and after NB-UVB treatment between the peripheral edge of lesional skin (PE skin) and the center of lesional ski...

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Main Authors: Suphagan Boonpethkaew, Jitlada Meephansan, Sasin Charoensuksira, Onjira Jumlongpim, Pattarin Tangtanatakul, Jongkonnee Wongpiyabovorn, Mayumi Komine, Akimichi Morita
Format: Article
Language:English
Published: Nature Portfolio 2023-03-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-023-31610-y
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author Suphagan Boonpethkaew
Jitlada Meephansan
Sasin Charoensuksira
Onjira Jumlongpim
Pattarin Tangtanatakul
Jongkonnee Wongpiyabovorn
Mayumi Komine
Akimichi Morita
author_facet Suphagan Boonpethkaew
Jitlada Meephansan
Sasin Charoensuksira
Onjira Jumlongpim
Pattarin Tangtanatakul
Jongkonnee Wongpiyabovorn
Mayumi Komine
Akimichi Morita
author_sort Suphagan Boonpethkaew
collection DOAJ
description Abstract Narrow band-ultraviolet B (NB-UVB) is an effective treatment for psoriasis. We aim to generate a potential mechanism of NB-UVB through comparing the transcriptomic profile before and after NB-UVB treatment between the peripheral edge of lesional skin (PE skin) and the center of lesional skin (CE skin) on the basis of molecular mechanisms of these two areas display different downstream functions. More than one-fourth of the NB-UVB-altered genes were found to be plaque-specific. Some of them were psoriasis signature genes that were downregulated by NB-UVB in, both, PE and CE skin (core alteration), such as IL36G, DEFB4A/B, S100A15, KRT16, and KRT6A. After NB-UVB treatment, the activity score of upstream cytokines, such as interferons, interleukin (IL)-6, IL-17, and IL-22 in pathogenesis decreased. In addition, NB-UVB could restore normal keratinization by upregulating LORICRIN and KRT2, particularly in the CE skin. Finally, we illustrated that NB-UVB is capable of suppressing molecules from the initiation to maintenance phase of plaque formation, thereby normalizing psoriatic plaques. This finding supports the usefulness of NB-UVB treatment in clinical practice and may help in the development of new treatment approaches in which NB-UVB treatment is included for patients with psoriasis or other inflammatory skin diseases.
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spelling doaj.art-5387cdbf10aa4deaa0bd207b3fdc63132023-11-19T13:00:23ZengNature PortfolioScientific Reports2045-23222023-03-0113111110.1038/s41598-023-31610-yElucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaquesSuphagan Boonpethkaew0Jitlada Meephansan1Sasin Charoensuksira2Onjira Jumlongpim3Pattarin Tangtanatakul4Jongkonnee Wongpiyabovorn5Mayumi Komine6Akimichi Morita7Division of Dermatology, Chulabhorn International College of Medicine, Thammasat UniversityDivision of Dermatology, Chulabhorn International College of Medicine, Thammasat UniversityDivision of Dermatology, Chulabhorn International College of Medicine, Thammasat UniversityDivision of Dermatology, Chulabhorn International College of Medicine, Thammasat UniversityDepartment of Transfusion Medicine and Clinical Microbiology, Faculty of Allied Health Sciences, Chulalongkorn UniversityDepartment of Microbiology, Faculty of Medicine, Center of Excellence in Immunology and Immune-Mediated Disease, Chulalongkorn UniversityDepartment of Dermatology, Jichi Medical UniversityDepartment of Geriatric and Environmental Dermatology, Nagoya City University Graduate School of Medical SciencesAbstract Narrow band-ultraviolet B (NB-UVB) is an effective treatment for psoriasis. We aim to generate a potential mechanism of NB-UVB through comparing the transcriptomic profile before and after NB-UVB treatment between the peripheral edge of lesional skin (PE skin) and the center of lesional skin (CE skin) on the basis of molecular mechanisms of these two areas display different downstream functions. More than one-fourth of the NB-UVB-altered genes were found to be plaque-specific. Some of them were psoriasis signature genes that were downregulated by NB-UVB in, both, PE and CE skin (core alteration), such as IL36G, DEFB4A/B, S100A15, KRT16, and KRT6A. After NB-UVB treatment, the activity score of upstream cytokines, such as interferons, interleukin (IL)-6, IL-17, and IL-22 in pathogenesis decreased. In addition, NB-UVB could restore normal keratinization by upregulating LORICRIN and KRT2, particularly in the CE skin. Finally, we illustrated that NB-UVB is capable of suppressing molecules from the initiation to maintenance phase of plaque formation, thereby normalizing psoriatic plaques. This finding supports the usefulness of NB-UVB treatment in clinical practice and may help in the development of new treatment approaches in which NB-UVB treatment is included for patients with psoriasis or other inflammatory skin diseases.https://doi.org/10.1038/s41598-023-31610-y
spellingShingle Suphagan Boonpethkaew
Jitlada Meephansan
Sasin Charoensuksira
Onjira Jumlongpim
Pattarin Tangtanatakul
Jongkonnee Wongpiyabovorn
Mayumi Komine
Akimichi Morita
Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
Scientific Reports
title Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
title_full Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
title_fullStr Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
title_full_unstemmed Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
title_short Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
title_sort elucidating the nb uvb mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
url https://doi.org/10.1038/s41598-023-31610-y
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