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Toxicité in vitro des particules atmosphériques fines et ultrafines : focus sur les bronchopneumopathies chroniques et la fonction mitochondriale

Abstract : Epidemiological studies have highlighted an association between ambient particulate matter (PM) level and hospital admissions or even mortality related with exacerbation of asthma and chronic obstructive pulmonary disease (COPD). While the role of inhaled PM in exacerbating these pathologies has been reported, pathophysiological mechanisms initiating and maintaining airway inflammation are not yet well understood. Reported health issues seems to be mostly caused by finest particles, due to their ability to diffuse deeply in the lungs, where clearance is less effective. Although numerous experimental studies demonstrated the toxicity of fine particles (PM2.5), mainly through oxidative stress-induced airway inflammation, only few studies have paid close attention to the ultrafine fraction (PM0.1), which attains new properties at nanometric scale. Because of its high specific surface area, PM0.1 is likely to be more biologically reactive. In this study, in vitro assays were conducted, exposing differentiated models of human bronchial epithelial cells (HBEC), from healthy, asthmatic and COPD-diseased donors, to one or three low dose of PM0.18-2.5 and PM0.18. Cytotoxicity, extracellular secretion of proinflammatory mediators and gene expression were studied. Furthermore, mitochondrion is a major endogenous source of reactive oxygen species (ROS) through oxidative metabolism, and coordinate many cell survival signaling processes. In this context, alterations in mitochondrial dynamic and function might play a key role in maintaining PM-induced oxidative stress and inflammation within lung cells, especially in case of chronic lung diseases initiation and/or exacerbation. Human bronchial epithelial BEAS-2B cells were also acutely or repeatedly exposed to low doses of fine (PM0.18-2.5) or ultrafine (PM0.18) particles, in order to characterize mitochondrial dynamic and function without massive cell death. Results highlighted in this study should contribute to a better understanding of the mechanisms governing the initiation and/or exacerbation of chronic airway lung diseases induced by air pollution-derived fine and ultra-fine PM.
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Submitted on : Wednesday, May 20, 2020 - 1:01:11 PM
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  • HAL Id : tel-02613773, version 1



Jules Sotty. Toxicité in vitro des particules atmosphériques fines et ultrafines : focus sur les bronchopneumopathies chroniques et la fonction mitochondriale. Médecine humaine et pathologie. Université du Droit et de la Santé - Lille II, 2019. Français. ⟨NNT : 2019LIL2S024⟩. ⟨tel-02613773⟩



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