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The inflammasome accelerates radiation-induced lung inflammation and fibrosis in mice

Authors
 Sung-Hwa Sohn  ;  Ji Min Lee  ;  Soojin Park  ;  Hyun Yoo  ;  Jeong Wook Kang  ;  Dasom Shin  ;  Kyung-Hwa Jung  ;  Yun-Sil Lee  ;  Jaeho Cho  ;  Hyunsu Bae 
Citation
 ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, Vol.39(2) : 917-926, 2015 
Journal Title
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
ISSN
 1382-6689 
Issue Date
2015
MeSH
Animals ; Antigens, CD/immunology ; Antigens, Differentiation, Myelomonocytic/immunology ; Bronchoalveolar Lavage Fluid/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Carrier Proteins/genetics* ; Caspase 1/genetics ; Cell Count ; Cytokines/genetics ; Cytokines/immunology ; Female ; Fibrosis ; Inflammasomes/genetics* ; Lung/pathology ; Mice, Inbred C57BL ; NLR Family, Pyrin Domain-Containing 3 Protein ; Pneumonia/immunology* ; Pneumonia/pathology ; Radiation Injuries, Experimental/immunology* ; Radiation Injuries, Experimental/pathology ; Vascular Cell Adhesion Molecule-1/genetics
Keywords
Fibrosis ; Inflammasome ; Pneumonitis ; Radiotherapy
Abstract
Although lung inflammation and fibrosis are well-documented dose-limiting side effects of lung irradiation, the mechanisms underlying these pathologies are unknown. An improved mechanistic understanding of radiation-induced pneumonitis is a prerequisite for the development of more effective radiotherapy; this was the rationale for the current study. Mouse lungs were focally irradiated with 75 Gy. The numbers of neutrophils, lymphocytes, macrophages, and total cells in the bronchoalveolar lavage fluid were counted, and pro-inflammatory cytokine levels were measured. Histological analysis and immunohistochemical staining for Tgf-β1 and Cd68 (a macrophage-specific protein) was also performed. After irradiation, mice developed pneumonitis, and exhibited higher numbers of neutrophils, lymphocytes, eosinophils, macrophages, and total cells compared to controls. In addition, inflammasome (Nlrp3, and caspase 1, Il1a, and Il1β), adhesion molecule (Vcam1), and cytokine (Il6) genes were significantly upregulated in the IR group. Cd68 and Tgfb1 proteins were significantly increased after irradiation. Upregulation of Cd68 and Tgfb1 correlates with the onset of radiation-induced pneumonitis and fibrosis. In addition, radiation-induced pneumonitis and fibrosis are accompanied by upregulation of phenotypic markers of inflammasome activity. Our findings have implications for the onset and exacerbation of damage in normal lung tissue.
Full Text
http://www.sciencedirect.com/science/article/pii/S1382668915000617
DOI
10.1016/j.etap.2015.02.019
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Sohn, Sung Hwa(손성화)
Cho, Jae Ho(조재호) ORCID logo https://orcid.org/0000-0001-9966-5157
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/139844
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