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김민정 이재면(미생물학교실) Allergy
등록일 : 2018-11-09 오후 12:13:00       조회 : 619
첨   부 :
제1저자 김민정(미생물학교실, BK21 신진연구인력), 심두희(미생물학교실)
교신저자 이재면(미생물학교실, BK21)

Allergy. 2018 Nov 7. doi: 10.1111/all.13661. [Epub ahead of print]
Chitinase 3-like 1 protein plays a critical role in RSV-induced airway inflammation.
Kim MJ1,2, Shim DH1, Cha HR1, Moon KY1, Yang CM1, Hwang SJ1, Kim KW2, Park JH1, Lee CG3, Elias JA3, Sohn MH2, Lee JM1.

Author information
1Department of Microbiology and Immunology, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Korea.2Department of Pediatrics, Severance Hospital, Institute of Allergy, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Korea.3Department of Molecular Microbiology and Immunology, Brown University, 185 Meeting Street, Box G-L, Providence, Rhode Island, 02912, USA.

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 is to investigate the relationship between CHI3L1 and airway inflammation caused by respiratory syncytial virus (RSV) infection.
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.
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, were 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.
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. This article is protected by copyright. All rights reserved.
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