汽车尾气中的微粒物质会改变人类 iPSC 衍生小胶质细胞的功能。

IF 7.2 1区 医学 Q1 TOXICOLOGY
Henna Jäntti, Steffi Jonk, Mireia Gómez Budia, Sohvi Ohtonen, Ilkka Fagerlund, Mohammad Feroze Fazaludeen, Päivi Aakko-Saksa, Alice Pebay, Šárka Lehtonen, Jari Koistinaho, Katja M Kanninen, Pasi I Jalava, Tarja Malm, Paula Korhonen
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引用次数: 0

摘要

背景:空气污染被认为是神经系统疾病的一个新兴环境风险因素。大规模流行病学研究表明,与交通相关的颗粒物(PM)会损害认知功能,并增加阿尔茨海默病等神经退行性疾病的发病率。吸入的可吸入颗粒物成分可能通过嗅觉途径直接侵入大脑,也可能通过外周系统反应导致大脑炎症和氧化应激。小胶质细胞是大脑的免疫细胞,与神经退行性疾病的进展有关联。然而,人们仍然不知道 PM 如何影响活的人类小胶质细胞:结果:我们在这里展示了两种不同的可吸入颗粒物,它们来自使用 EN590 柴油或压缩天然气(CNG)的汽车尾气,会改变体外人类小胶质细胞的功能。我们将人类诱导多能干细胞(iPSC)衍生的小胶质细胞(iMGLs)暴露于与交通相关的可吸入颗粒物中,并探索了它们的功能反应。10 至 100 µg ml-1 的低浓度可吸入颗粒物可提高小胶质细胞的存活率,而较高浓度的可吸入颗粒物则会随着时间的推移而产生毒性。与脂多糖诱导的反应相比,两种测试污染物都会损害小胶质细胞的吞噬功能,并以不同的模式增加一些促炎细胞因子的分泌。iMGLs对活性氧(ROS)的产生表现出污染物依赖性反应,CNG会诱导ROS的产生,而EN590则会减少ROS的产生:我们的研究表明,与交通相关的空气污染物会改变人类小胶质细胞的功能,因此有必要进行进一步研究,以确定这些变化是否会随着时间的推移对大脑和认知能力产生不利影响。这项研究表明,人类 iPSC-小胶质细胞是研究小胶质细胞对环境因素的功能性反应的重要工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Particulate matter from car exhaust alters function of human iPSC-derived microglia.

Background: Air pollution is recognized as an emerging environmental risk factor for neurological diseases. Large-scale epidemiological studies associate traffic-related particulate matter (PM) with impaired cognitive functions and increased incidence of neurodegenerative diseases such as Alzheimer's disease. Inhaled components of PM may directly invade the brain via the olfactory route, or act through peripheral system responses resulting in inflammation and oxidative stress in the brain. Microglia are the immune cells of the brain implicated in the progression of neurodegenerative diseases. However, it remains unknown how PM affects live human microglia.

Results: Here we show that two different PMs derived from exhausts of cars running on EN590 diesel or compressed natural gas (CNG) alter the function of human microglia-like cells in vitro. We exposed human induced pluripotent stem cell (iPSC)-derived microglia-like cells (iMGLs) to traffic related PMs and explored their functional responses. Lower concentrations of PMs ranging between 10 and 100 µg ml-1 increased microglial survival whereas higher concentrations became toxic over time. Both tested pollutants impaired microglial phagocytosis and increased secretion of a few proinflammatory cytokines with distinct patterns, compared to lipopolysaccharide induced responses. iMGLs showed pollutant dependent responses to production of reactive oxygen species (ROS) with CNG inducing and EN590 reducing ROS production.

Conclusions: Our study indicates that traffic-related air pollutants alter the function of human microglia and warrant further studies to determine whether these changes contribute to adverse effects in the brain and on cognition over time. This study demonstrates human iPSC-microglia as a valuable tool to study functional microglial responses to environmental agents.

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来源期刊
CiteScore
15.90
自引率
4.00%
发文量
69
审稿时长
6 months
期刊介绍: Particle and Fibre Toxicology is an online journal that is open access and peer-reviewed. It covers a range of disciplines such as material science, biomaterials, and nanomedicine, focusing on the toxicological effects of particles and fibres. The journal serves as a platform for scientific debate and communication among toxicologists and scientists from different fields who work with particle and fibre materials. The main objective of the journal is to deepen our understanding of the physico-chemical properties of particles, their potential for human exposure, and the resulting biological effects. It also addresses regulatory issues related to particle exposure in workplaces and the general environment. Moreover, the journal recognizes that there are various situations where particles can pose a toxicological threat, such as the use of old materials in new applications or the introduction of new materials altogether. By encompassing all these disciplines, Particle and Fibre Toxicology provides a comprehensive source for research in this field.
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