Pajarskienė Justina, Vailionytė Agnė, Uogintė Ieva, Byčenkienė Steigvilė, Jonavičė Ugnė, Uzielienė Ilona, Bagdonas Edvardas, Aldonytė Rūta
Department of Regenerative Medicine, State Research Institute Centre for Innovative Medicine, Santariškių st. 5, 08406, Vilnius, Lithuania.
Department of Environmental Research, State Research Institute Center for Physical Sciences and Technology, Saulėtekio av. 3, 10257, Vilnius, Lithuania.
Arch Toxicol. 2025 Feb;99(2):787-796. doi: 10.1007/s00204-024-03909-w. Epub 2024 Nov 29.
Carbon black is a key component of air-borne particulate matter, linked to adverse health outcomes, such as increased susceptibility to respiratory infections and chronic pulmonary disease exacerbations. Fine and ultrafine particles can penetrate the lungs, enter the bloodstream, and induce pathogenetic events. Macrophages play a crucial role in responding to inhaled particles, including carbon black, by initiating an innate immune response and upregulating pro-inflammatory cytokines and anti-oxidative enzymes. This study investigates the effects of carbon black particles on human monocyte-derived macrophages in vitro at a concentration of 10 µg/ml, offering insights into their potential role in disease pathogenesis. We have compared two commercially available carbon black particle types using various physicochemical techniques and assessed their biological effects on monocyte-derived macrophages. We have evaluated changes in cell viability, morphology, and particle uptake/phagocytosis. Western blot, ELISA, and RT-qPCR measured inflammatory and oxidative stress biomarkers. Both types of carbon black particles induced similar responses in macrophages, including particle uptake, cytokine production, and oxidative stress-related protein expression. The observed changes suggest activation of the Nrf2-mediated antioxidant response, impaired autophagy, and decreased cellular defense against oxidative stress, indicating potential pathways for chronic inflammatory lung disease development.
炭黑是空气传播颗粒物的关键成分，与不良健康后果相关，如呼吸道感染易感性增加和慢性肺病急性加重。细颗粒和超细颗粒可穿透肺部，进入血液，并引发致病事件。巨噬细胞在对吸入颗粒（包括炭黑）的反应中起关键作用，通过启动固有免疫反应并上调促炎细胞因子和抗氧化酶。本研究在体外以10μg/ml的浓度研究炭黑颗粒对人单核细胞衍生巨噬细胞的影响，以深入了解其在疾病发病机制中的潜在作用。我们使用各种物理化学技术比较了两种市售炭黑颗粒类型，并评估了它们对单核细胞衍生巨噬细胞的生物学效应。我们评估了细胞活力、形态以及颗粒摄取/吞噬作用的变化。蛋白质免疫印迹法、酶联免疫吸附测定法和逆转录定量聚合酶链反应测定了炎症和氧化应激生物标志物。两种类型的炭黑颗粒在巨噬细胞中诱导了相似的反应，包括颗粒摄取、细胞因子产生和氧化应激相关蛋白表达。观察到的变化表明Nrf2介导的抗氧化反应激活、自噬受损以及细胞对氧化应激的防御能力下降，提示了慢性炎症性肺病发展的潜在途径。
