Pulmonary, Critical Care, Sleep and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska 68198.
Division of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, California 92521.
Toxicol Sci. 2018 Apr 1;162(2):635-644. doi: 10.1093/toxsci/kfx286.
Agricultural organic dust exposures trigger harmful airway inflammation, and workers experiencing repetitive dust exposures are at increased risk for lung disease. Mesenchymal stem/stromal cells (MSCs) regulate wound repair processes in the lung, and may contribute to either proresolution or -fibrotic lung responses. It is unknown how organic dust exposures alter lung-resident MSC activation and proinflammatory versus prorepair programs in the lung. To address this gap in knowledge, we isolated human lung-resident MSC from lung tissue. Cells were stimulated with aqueous extracts of organic dusts (DE) derived from swine confinement facilities and were assessed for changes in proliferative and migratory capacities, and production of proinflammatory and prorepair mediators. Through these investigations, we found that DE induces significant release of proinflammatory mediators TNF-α, IL-6, IL-8, and matrix metalloproteases, while also inducing the production of prorepair mediators amphiregulin, FGF-10, and resolvin D1. In addition, DE significantly reduced the growth and migratory capacities of lung-resident MSC. Together, these investigations indicate lung-resident MSC activation and wound repair activities are altered by organic dust exposures. These findings warrant future investigations to assess how organic dusts affect lung-resident mesenchymal stem/stromal cell function and impact airway inflammation, injury, and repair during agricultural aerosol exposures.
农业性有机粉尘暴露会引发有害的气道炎症,而反复接触粉尘的工人患肺病的风险增加。间充质干细胞/基质细胞 (MSCs) 调节肺部的伤口修复过程,可能有助于肺部的促缓解或促纤维化反应。目前尚不清楚有机粉尘暴露如何改变肺部驻留 MSC 的激活以及肺部的促炎与促修复程序。为了填补这一知识空白,我们从肺组织中分离出了人肺驻留 MSC。用来自猪舍的有机粉尘 (DE) 的水提物刺激细胞,并评估其增殖和迁移能力以及促炎和促修复介质的产生变化。通过这些研究,我们发现 DE 可显著诱导 TNF-α、IL-6、IL-8 和基质金属蛋白酶等促炎介质的释放,同时还可诱导促修复介质 Amphiregulin、FGF-10 和 Resolvin D1 的产生。此外,DE 还显著降低了肺驻留 MSC 的生长和迁移能力。总之,这些研究表明,有机粉尘暴露会改变肺驻留 MSC 的激活和伤口修复活性。这些发现需要进一步研究,以评估有机粉尘如何影响肺驻留间充质干细胞/基质细胞的功能,并在农业气溶胶暴露期间影响气道炎症、损伤和修复。