The role of Interleukin 15 in protein degradation in skeletal muscles in rats of chronic obstructive pulmonary disease.

AIM: The present study aimed to investigate the role of Interleukin 15 (IL-15) in protein degradation in skeletal muscle mediated by the ubiquitin-proteasome pathway (UPP) in a rat model of chronic obstructive pulmonary disease (COPD).

METHODS

The COPD model was established in 30 Sprague Dawley (SD) rats through the combination of passive smoking and intratracheal injection of lipopolysaccharide (LPS). The pathological changes in lungs and bronchi of COPD rats (n=30) were compared with that of control rats (n=15). The levels of IL-15 and tumor necrosis factor-α (TNF- α) in the serum, diaphragm, gastrocnemius, and the intercostal muscles were measured using enzyme-linked immunosorbent assay (ELISA), and compared between the COPD and control rats. In addition, the expression of E2-14K, MAFbx, and ubiquitin (Ub) was evaluated using quantitative real-time PCR and western blot and compared between the COPD and control rats.

RESULTS

The levels of IL-15 and TNF-α in the serum, diaphragm, gastrocnemius, and the intercostal muscles in COPD rats were significantly higher than that in control rats. The expression of E2-14K, MAFbx, and ubiquitin (Ub) in the diaphragm, gastrocnemius, and the intercostal muscles in COPD rats was also significantly higher than that in the control rats. In addition, we identified positive correlation between the levels of IL-15 and TNF-α. Positive correlation was also identified between the levels of IL-15 and E2-14K, MAFbx, and Ub.

CONCLUSION

Our results suggest that IL-15 inhibited the protein degradation in skeletal muscle in COPD rats, which may be mediated by the TNF-α and UPP pathway.