The progression of comorbidity in IL-18 transgenic chronic obstructive pulmonary disease mice model |
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Authors: | Shin-ichi Takenaka Tomotaka Kawayama Haruki Imaoka Yuki Sakazaki Hanako Oda Yoichiro Kaku Masanobu Matsuoka Masaki Okamoto Seiya Kato Kentaro Yamada Tomoaki Hoshino |
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Institution: | 1. Division of Respirology, Neurology and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan;2. Division of Pathology and Cell Biology, Graduate School and Faculty of Medicine, University of the Ryukyus, Okinawa 903-0215, Japan;3. Division of Endocrinology and Metabolism, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan |
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Abstract: | 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. |
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Keywords: | IL-18 IL-13 COPD Transgenic mouse |
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