Interleukin-17A Deficiency Attenuated Emphysema and Bone Loss in Mice Exposed to Cigarette Smoke.

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.