Siriphorn Siriporn Vongsaiyat, Thorsuwan Supitsara, Thongam Julalux, Ruangklai Sukpattaraporn, Hussarin Poungpetch, Rungruang Thanaporn, Srisuma Sorachai
Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Faculty of Physical Therapy and Sports Medicine, Rangsit University, Pathumtani, Thailand.
COPD. 2025 Mar 6;22(1):2477235. doi: 10.1080/15412555.2025.2477235. Epub 2025 Mar 13.
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.
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.
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.
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 findings. Elevated adiponectin expression in alveolar epithelial cells suggests its potential role in the development of COPD by enhancing lung inflammation.
香烟烟雾可引发肺部炎症、破坏以及慢性阻塞性肺疾病（COPD）的发展。在受肺部炎症影响的各种因素中，肺上皮细胞产生的脂联素被认为在调节炎症和维持组织完整性方面发挥着重要作用。本研究旨在检测香烟烟雾提取物（CSE）诱导的肺气肿小鼠模型中脂联素的表达，并探讨脂联素对CSE诱导的肺上皮细胞损伤中细胞存活和细胞因子基因表达的影响。
通过使香烟烟雾通过装有溶剂的玻璃管来制备CSE。将磷酸盐缓冲液（PBS）或CSE腹腔注射到C57BL/6小鼠体内。评估肺部、支气管肺泡灌洗液（BALF）和脂肪组织中的炎症细胞、细胞因子、脂联素表达。将CSE和脂联素施用于A549细胞以确定细胞活力和细胞因子基因表达。
腹腔注射CSE可使平均肺泡线性截距显著增加23.11%。CSE可显著增加BALF中的总细胞、巨噬细胞、中性粒细胞、嗜酸性粒细胞、肿瘤坏死因子α（TNFα）、白细胞介素1β（IL-1β）水平。CSE可增强肺部脂联素蛋白表达。用CSE处理A549细胞会降低细胞存活率和脂联素基因表达。此外，脂联素处理可增强CSE暴露后A549细胞中单核细胞趋化蛋白1（MCP-1）和白细胞介素8（IL-8）基因表达。
腹腔注射CSE可诱导小鼠肺部炎症、气腔扩大并增加脂联素表达。暴露于CSE的A549细胞显示细胞活力降低、促炎基因上调、脂联素基因下调。脂联素处理进一步增强了这些基因的表达，与研究结果一致。肺泡上皮细胞中脂联素表达升高表明其可能通过增强肺部炎症在COPD发展中发挥作用。
