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Chitinase 3-like 1 drives allergic skin inflammation via Th2 immunity and M2 macrophage activation

 Eun Ji Kwak  ;  Jung Yeon Hong  ;  Mi Na Kim  ;  Soo Yeon Kim  ;  Seo Hyeong Kim  ;  Chang Ook Park  ;  Kyung Won Kim  ;  Chun Geun Lee  ;  Jack A. Elias  ;  Hye Mi Jee  ;  Myung Hyun Sohn 
 CLINICAL AND EXPERIMENTAL ALLERGY, Vol.49(11) : 1464-1474, 2019 
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atopic dermatitis ; chitinase 3-like 1 ; skin barrier ; type 2 immunity
BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by defective skin barrier and Th2 immune responses. Chitinase 3-like 1 (CHI3L1), also known as breast regression protein 39 (BRP-39) in mice and human homologue YKL-40, plays important roles in Th2 inflammation and allergen sensitization. CHI3L1 has been implicated in a variety of diseases including asthma characterized by inflammation, apoptosis and tissue remodelling, but its role in AD remains elusive. OBJECTIVE: The aim of this study was to investigate the role of CHI3L1 in the development and progression of AD. RESULTS: We investigated YKL-40 levels in the serum and skin of AD patients by ELISA and immunofluorescence, respectively. Using a murine model of AD induced by ovalbumin (OVA), we investigated Th2 immune responses, M2 macrophage activation and skin barrier gene expression using wild-type (WT) and BRP-39 null mutant (BRP-39-/- ) mice. YKL-40 level was significantly increased in serum of AD patients. In addition, both mRNA and protein expression levels of BRP-39 were higher in OVA-sensitized WT mice than in control mice. OVA-sensitized BRP-39-/- mice showed decreased epidermal thickness, lower total serum IgE, Th2 cytokine levels and CD4+ effector T cell populations than OVA-sensitized WT mice. Induction of BRP-39 was dominant in dermal macrophages. BRP-39 deficiency was found to be involved in M2 macrophage activation. Consistently, the YKL-40 level in the skin of AD patients was higher than in normal subjects and it was expressed in dermal macrophages. BRP-39 deficiency attenuated dysregulation of skin barrier and tight junction genes. CONCLUSIONS AND CLINICAL RELEVANCE: These findings demonstrate that CHI3L1 mediates the development of AD induced by OVA, affecting Th2 inflammation, M2 macrophage activation and skin barrier function.
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1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아청소년과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
7. Others (기타) > Others (기타) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Won(김경원) ORCID logo https://orcid.org/0000-0003-4529-6135
Kim, Mina(김미나) ORCID logo https://orcid.org/0000-0002-1675-0688
Kim, Soo Yeon(김수연) ORCID logo https://orcid.org/0000-0003-4965-6193
Park, Chang Ook(박창욱) ORCID logo https://orcid.org/0000-0003-3856-1201
Sohn, Myung Hyun(손명현) ORCID logo https://orcid.org/0000-0002-2478-487X
Hong, Jung Yeon(홍정연) ORCID logo https://orcid.org/0000-0003-0406-9956
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