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Chitinase 3-like 1 protein plays a critical role in respiratory syncytial virus-induced airway inflammation

 Min Jung Kim  ;  Doo Hee Shim  ;  Hye‐Ran Cha  ;  Kuk‐Young Moon  ;  Chang Mo Yang  ;  Su Jin Hwang  ;  Kyung Won Kim  ;  Jeon Han Park  ;  Chun Geun Lee  ;  Jack A. Elias  ;  Myung Hyun Sohn  ;  Jae Myun Lee 
 ALLERGY, Vol.74(4) : 685-697, 2019 
Journal Title
Issue Date
bronchiolitis ; chitinase 3-like 1 protein ; lower respiratory tract infection ; respiratory syncytial viruses ; type 2 immunity
BACKGROUND: Chitinase 3-like 1 protein (CHI3L1) (YKL-40 in humans and breast regression protein [BRP]-39 in mice) is required for optimal allergen sensitization and Th2 inflammation in various chronic inflammatory diseases including asthma. However, the role of CHI3L1 in airway inflammation induced by respiratory viruses has not been investigated. The aim of this study was to investigate the relationship between CHI3L1 and airway inflammation caused by respiratory syncytial virus (RSV) infection. METHODS: We measured YKL-40 levels in human nasopharyngeal aspirate (NPA) from hospitalized children presenting with acute respiratory symptoms. Wild-type (WT) and BRP-39 knockout (KO) C57BL/6 mice were inoculated with live RSV (A2 strain). Bronchoalveolar lavage fluid and lung tissue samples were obtained on day 7 after inoculation to assess lung inflammation, airway reactivity, and expression of cytokines and BRP-39. RESULTS: In human subjects, YKL-40 and IL-13 levels in NPA were higher in children with RSV infection than in control subjects. Expression of BRP-39 and Th2 cytokines, IL-13 in particular, was increased following RSV infection in mice. Airway inflammation caused by RSV infection was reduced in BRP-39 KO mice as compared to WT mice. Th2 cytokine levels were not increased in the lungs of RSV-infected BRP-39 KO mice. BRP-39 regulated M2 macrophage activation in RSV-infected mice. Additionally, treatment with anti-CHI3L1 antibody attenuated airway inflammation and Th2 cytokine production in RSV-infected WT mice. CONCLUSION: These findings suggest that CHI3L1 could contribute to airway inflammation induced by RSV infection. CHI3L1 could be a potential therapeutic candidate for attenuating Th2-associated immunopathology during RSV infection.
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아청소년과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Won(김경원) ORCID logo https://orcid.org/0000-0003-4529-6135
Kim, Min Jung(김민정) ORCID logo https://orcid.org/0000-0002-5634-9709
Park, Jeon Han(박전한) ORCID logo https://orcid.org/0000-0001-9604-3205
Sohn, Myung Hyun(손명현) ORCID logo https://orcid.org/0000-0002-2478-487X
Shim, Doo Hee(심두희) ORCID logo https://orcid.org/0000-0002-6696-7199
Lee, Jae Myun(이재면) ORCID logo https://orcid.org/0000-0002-5273-3113
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