Upregulated IGF‑1 in the lungs of asthmatic mice originates from alveolar macrophages.

Asthma is characterized by inflammation and remodeling of the airways. Insulin‑like growth factor-1 (IGF‑1) serves an important role in the repair of lung tissue injury and airway remodeling by elevating collagen and elastin content, increasing the thickness of smooth muscle and promoting the proliferation of lung epithelial and interstitial cells, as well as fibroblasts; however, the content of IGF‑1 and its cellular origin in the lungs of patients with asthma remain unknown. In the present study, a mouse model of asthma was constructed. Following isolation of alveolar macrophages (AMs), the content of IGF‑1 in lung tissue and bronchoalveolar lavage fluid (BALF) was detected by ELISA. The proliferation and phagocytosis of alveolar epithelial cells (AECs) stimulated by IGF‑1 were detected by Cell Counting Kit‑8 method and flow cytometry, respectively. In the present study, IGF‑1 was upregulated in the lung tissues of asthmatic mice, and the content of IGF‑1 in BALF was also elevated. Depletion of AMs by treating mice with 2‑chloroadenosine via nose dripping reversed the increase of IGF‑1 by 80% in lung tissues and by ~100% in BALF of asthmatic mice, suggesting that elevated IGF‑1 in asthmatic mice predominantly originated from AMs. As IGF‑1 promotes the proliferation and phagocytosis of AECs, AM‑derived IGF‑1 may serve an important role in the regulation of airway inflammation and remodeling in asthmatic mice.