| First Author | Takenaka S | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 445 |
| Issue | 3 | Pages | 597-601 |
| PubMed ID | 24565845 | Mgi Jnum | J:219136 |
| Mgi Id | MGI:5619695 | Doi | 10.1016/j.bbrc.2014.02.052 |
| Citation | Takenaka S, et al. (2014) The progression of comorbidity in IL-18 transgenic chronic obstructive pulmonary disease mice model. Biochem Biophys Res Commun 445(3):597-601 |
| abstractText | Patients with severe COPD are known to have comorbidities such as emaciation, cor pulmonale and right heart failure, muscle weakness, hyperlipemia, diabetes mellitus, osteoporosis, muscle atrophy, arterial sclerosis, hypertension, and depression. Therefore, treatment for COPD needs to focus on these comorbidities as well as the lungs. We previously reported a new mouse model of COPD utilizing the human surfactant protein C promoter SP-C to drive the expression of mature mouse IL-18 cDNA; constitutive IL-18 overproduction in the lungs of transgenic (Tg) mice induces severe emphysematous change, dilatation of the right ventricle, and mild pulmonary hypertension with aging. In the present study, we evaluated the progression of comorbidity in our COPD model. In female Tg mice, significant weight loss was observed at 16 weeks and beyond, when compared with control wild-type (WT) mice. This weight loss was suppressed in IL-13-deficient (knockout; KO) Tg mice. Muscle weight and bone mineral density were significantly decreased in aged Tg mice relative to control WT and IL-13 KO Tg mice. The aged Tg mice also showed impaired glucose tolerance. IL-18 and IL-13 may play important roles in the pathogenesis of comorbidity in COPD patients. |
