| First Author | Xiong J | Year | 2020 |
| Journal | Int J Chron Obstruct Pulmon Dis | Volume | 15 |
| Pages | 301-310 | PubMed ID | 32103929 |
| Mgi Jnum | J:302476 | Mgi Id | MGI:6508197 |
| Doi | 10.2147/COPD.S235384 | Citation | Xiong J, et al. (2020) Interleukin-17A Deficiency Attenuated Emphysema and Bone Loss in Mice Exposed to Cigarette Smoke. Int J Chron Obstruct Pulmon Dis 15:301-310 |
| abstractText | 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-kappaB 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-1beta 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. |
