COPD · 2025
Alterations in Adiponectin Expression in Models of Cigarette Smoke Extract-Induced Mouse Pulmonary Emphysema and Alveolar Epithelial Cell Injury.
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Siriphorn Siriporn Vongsaiyat, Thorsuwan Supitsara, Thongam Julalux, Ruangklai Sukpattaraporn, Hussarin Poungpetch, Rungruang Thanaporn, Srisuma Sorachai
Аннотация
PURPOSE: Cigarette smoke activates lung inflammation and destruction and the development of COPD. Among various factors influenced by lung inflammation, adiponectin produced by lung epithelial cells is thought to play a significant role in regulating inflammation and maintaining tissue integrity. This study aims to examine adiponectin expression in a mouse model of cigarette smoke extract (CSE)-induced emphysema and explore the effects of adiponectin on cell survival and cytokine gene expression in CSE-induced lung epithelial cell damage.
METHODS: CSE was prepared by passing cigarette smoke through a glass tube containing solvent. PBS or CSE was intraperitoneally administered to C57BL/6 mice. Inflammatory cells, cytokines, adiponectin expression in lung, bronchoalveolar lavage fluid (BALF) and adipose tissue were assessed. CSE and adiponectin were administered to A549 cells to determine cell viability and cytokine gene expression.
RESULTS: Intraperitoneal CSE injection significantly increased the mean alveolar linear intercept by 23.11%. CSE significantly increased total cells, macrophages, neutrophils, eosinophils, TNFα, IL-1β levels in BALF. CSE enhanced lung adiponectin protein expression. Treatment of A549 cells with CSE reduced cell survival and adiponectin gene expression. Furthermore, adiponectin treatment enhanced MCP-1 and IL-8 gene expression in A549 cells post-CSE exposure.
CONCLUSION: Intraperitoneal CSE treatment induced lung inflammation, airspace enlargement, and increased adiponectin expression in mice. CSE-exposed A549 cells showed reduced cell viability, upregulated proinflammatory genes, downregulated adiponectin genes. Adiponectin treatment further intensified these genes expressions, aligning with in vivo findings. Elevated adiponectin expression in alveolar epithelial cells suggests its potential role in the development of COPD by enhancing lung inflammation.
METHODS: CSE was prepared by passing cigarette smoke through a glass tube containing solvent. PBS or CSE was intraperitoneally administered to C57BL/6 mice. Inflammatory cells, cytokines, adiponectin expression in lung, bronchoalveolar lavage fluid (BALF) and adipose tissue were assessed. CSE and adiponectin were administered to A549 cells to determine cell viability and cytokine gene expression.
RESULTS: Intraperitoneal CSE injection significantly increased the mean alveolar linear intercept by 23.11%. CSE significantly increased total cells, macrophages, neutrophils, eosinophils, TNFα, IL-1β levels in BALF. CSE enhanced lung adiponectin protein expression. Treatment of A549 cells with CSE reduced cell survival and adiponectin gene expression. Furthermore, adiponectin treatment enhanced MCP-1 and IL-8 gene expression in A549 cells post-CSE exposure.
CONCLUSION: Intraperitoneal CSE treatment induced lung inflammation, airspace enlargement, and increased adiponectin expression in mice. CSE-exposed A549 cells showed reduced cell viability, upregulated proinflammatory genes, downregulated adiponectin genes. Adiponectin treatment further intensified these genes expressions, aligning with in vivo findings. Elevated adiponectin expression in alveolar epithelial cells suggests its potential role in the development of COPD by enhancing lung inflammation.