Interleukin-17A Deficiency Attenuated Emphysema and Bone Loss in Mice Exposed to Cigarette Smoke
Authors Xiong J, Tian J, Zhou L, Le Y, Sun Y
Received 20 October 2019
Accepted for publication 22 January 2020
Published 10 February 2020 Volume 2020:15 Pages 301—310
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Chunxue Bai
Jing Xiong,1 Jieyu Tian,2 Lu Zhou,1 Yanqing Le,1 Yongchang Sun1
1Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, 100191, People’s Republic of China; 2Hematology Oncology Center, Beijing Children’s Hospital, Capital Medical University, Beijing 100045, People’s Republic of China
Correspondence: Yongchang Sun
Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing 100191, People’s Republic of China
Tel +86 156 1196 3697
Email [email protected]
Background and Purpose: Chronic obstructive pulmonary disease (COPD) is a common chronic inflammatory disease, which is associated with various comorbidities including osteoporosis. Interleukin(IL)-17 has been reported to play important roles in the pathogenesis of COPD and also associated with bone destruction in inflammatory diseases. However, the role of IL-17A in COPD-related osteoporosis is yet unknown. The purpose of our study was to investigate the potential contribution of IL-17A in COPD-related bone loss.
Materials and Methods: We examined the bone mass and bone microarchitecture in wild-type and IL-17A-/- mice exposed to long-term cigarette smoke (CS). Osteoclast activities and the expression of receptor activator of nuclear factor-κB ligand (RANKL) in bone tissues were assessed, and the blood levels of inflammatory cytokines were measured.
Results: Less bone loss as well as attenuated emphysema were shown in IL-17A-/- mice compared with wild-type mice. CS-exposed IL-17A-/- mice had decreased TRAP+ osteoclast numbers and lower RANKL expression compared with CS-exposed wild-type mice. Inflammatory cytokines including IL-6 and IL-1β in circulation were decreased in IL-17A-/- mice exposed to CS compared with wild-type mice.
Conclusion: This study indicates that IL-17A is involved in CS-induced bone loss and may be a common link between COPD and osteoporosis.
Keywords: chronic obstructive pulmonary disease, osteoporosis, interleukin 17, receptor activator of nuclear factor-κB ligand
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