Alsohime Fahad, Saheb Sharif-Askari Narjes, Alharbi Nasser Saleh, Alosaimi Mohammed Faraj Ayad, Halwani Rabih
Pediatric Department, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Pediatric critical care unit, King Saud University Medical City, Riyadh, Saudi Arabia.
PLoS One. 2025 Aug 22;20(8):e0330762. doi: 10.1371/journal.pone.0330762. eCollection 2025.
Smoking could potentiate the profibrotic effects of silica in the lungs, including increasing the risk of cancer and silicosis. Crystalline silica-induced silicosis has been associated with lung fibrosis. Moreover, smoking is strongly linked with an increased risk of idiopathic pulmonary fibrosis. Although pulmonary fibrosis is a recognized feature in asthma airway modeling, the effects of cigarette smoke and silica, both individually and together, have not been studied. We examined the effect of cigarette smoke extract (CSE) on silica-induced fibrosis in asthmatic patients and healthy individuals by using fibroblasts from both groups. Cigarette smoke enhanced the fibrotic effects of silica in healthy and asthmatic lung fibroblasts. Healthy fibroblasts exhibited low baseline levels of fibrotic proteins. However, exposure to CSE and silica significantly increased extracellular matrix (ECM) markers. Asthmatic fibroblasts, with higher baseline levels of these markers, showed even greater upregulation upon exposure. The combination of silica and cigarette smoke also promoted collagen deposition and upregulated levels of matrix metalloproteinases (MMPs) and their inhibitors (TIMP-1 and TIMP-2) in asthmatic fibroblasts. Cessation of smoking and control of silica exposure are essential for reducing lung inflammation and fibrosis. Additionally, therapeutic targets should be investigated for their protective effects against these toxins.
吸烟可能会增强二氧化硅在肺部的促纤维化作用，包括增加患癌和矽肺病的风险。结晶二氧化硅诱发的矽肺病与肺纤维化有关。此外，吸烟与特发性肺纤维化风险增加密切相关。虽然肺纤维化是哮喘气道模型中的一个公认特征，但香烟烟雾和二氧化硅各自以及共同的影响尚未得到研究。我们通过使用两组的成纤维细胞，研究了香烟烟雾提取物（CSE）对哮喘患者和健康个体中二氧化硅诱导的纤维化的影响。香烟烟雾增强了二氧化硅对健康和哮喘肺成纤维细胞的纤维化作用。健康的成纤维细胞表现出较低的纤维化蛋白基线水平。然而，暴露于CSE和二氧化硅会显著增加细胞外基质（ECM）标志物。这些标志物基线水平较高的哮喘成纤维细胞在暴露后表现出更大程度的上调。二氧化硅和香烟烟雾的组合还促进了哮喘成纤维细胞中的胶原蛋白沉积，并上调了基质金属蛋白酶（MMPs）及其抑制剂（TIMP - 1和TIMP - 2）的水平。戒烟和控制二氧化硅暴露对于减少肺部炎症和纤维化至关重要。此外，应研究治疗靶点对这些毒素的保护作用。
