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강민종 (Min-Jong Kang) 저자 이메일 보기
Yale University School of Medicine
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조회 3320  인쇄하기 주소복사 트위터 공유 페이스북 공유 
IL-18 Induces Emphysema, and Airway and Vascular Remodeling via IFN-γ, IL-17A and IL-13

Min-Jong Kang1,* , Je-Min Choi2,3,*, Bo Hye Kim1, Chang-Min Lee1, Won-Kyung Cho1, Gina Choe1, Do-Hyun Kim2,3, Chun Geun Lee1 and Jack A Elias1,4,5

1Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine
2Department of Life Science, Research Institute for Natural Sciences,
3Hanyang Biomedical Research Institute,Hanyang University, Seoul, 133-791, Republic of Korea
4Department of Internal Medicine, Yale University School of Medicine
5Corresponding Author: Jack A Elias
*Equally contributed for the study

Abstract
Rationale. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation, alveolar destruction and airway and vascular remodeling. However, the mechanism(s) that leads to these diverse alterations has not been defined.

Hypothesis. We hypothesized that IL-18 plays a central role in the pathogenesis of these lesions.

Methods. We generated and characterized lung-specific, inducible IL-18 transgenic mice.

Results. Here we demonstrate that the expression of IL-18 in the mature murine lung induces inflammation that is associated with the accumulation of CD4+, CD8+, CD19+ and NK1.1+ cells, emphysema, mucus metaplasia, airway fibrosis, vascular remodeling and right ventricle cardiac hypertrophy. We also demonstrate that IL-18 induces type 1, type 2 and type 17 cytokines with gamma interferon (IFN-γ) inhibiting macrophage, lymphocyte and eosinophil accumulation while stimulating alveolar destruction and genes associated with cell cytotoxicity and IL-13 and IL-17A inducing mucus metaplasia, airway fibrosis, and vascular remodeling. We also highlight interactions between these responses with IL-18 inducing IL-13 via an IL-17A-dependent mechanism and the type 1 and type17/type 2 responses counterregulating each another.

Conclusions. These studies define the spectrum of inflammatory, parenchymal, airway and vascular alterations that are induced by pulmonary IL-18, highlight the similarities between these responses and the lesions in COPD and define the selective roles that type 1, type 2 and type 17 responses play in the generation of IL-18-induced pathologies.

interleukin-18, chronic obstuctive pulmonary disease, airway fibrosis, vascular remodeling, cor pulmonale

논문정보 F1000선정
- 형식: Research article
- 게재일: 2012년 03월 (BRIC 등록일 2012-03-06)
- 연구진: 국내+국외 연구진
- 분야: Medicine
Dot/Icm 제 4 유형 커플링 단백질 복합체의 선택적 이펙터 단백질 인식[Nat. Commun.]
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발표: 김현민 (KAIST)
일자: 2020년 9월 29일 (화) 오후 02시 (한국시간)
언어: 한국어
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