Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Oxidative stress and inflammation induced by air pollution-derived PM2.5 persist in the lungs of mice after cessation of their sub-chronic exposure
https://orcid.org/0009-0008-9768-378X
https://orcid.org/0009-0001-9186-0764
https://orcid.org/0000-0001-5572-0871
https://orcid.org/0000-0002-5179-1311
Graphical abstract Display Omitted
Highlights Outdoor air PM2.5 had intrinsic OP related to their physico-chemical characteristics. Intrinsic OP of outdoor air PM2.5 predicted induction of oxidative stress in lungs. Nrf2 and NFκB cell signaling pathways were activated by outdoor air PM2.5 in lungs. Oxidative and inflammatory effects persisted in lungs despite exposure cessation. Better knowledge of the persistence of outdoor air PM2.5-induced lung toxicity.
Abstract More than 7 million early deaths/year are attributable to air pollution. Current health concerns are especially focused on air pollution-derived particulate matter (PM). Although oxidative stress-induced airway inflammation is one of the main adverse outcome pathways triggered by air pollution-derived PM, the persistence of both these underlying mechanisms, even after exposure cessation, remained poorly studied. In this study, A/JOlaHsd mice were also exposed acutely (24 h) or sub-chronically (4 weeks), with or without a recovery period (12 weeks), to two urban PM2.5 samples collected during contrasting seasons (i.e., autumn/winter, AW or spring/summer, SS). The distinct intrinsic oxidative potentials (OPs) of AW and SS PM2.5, as evaluated in acellular conditions, were closely related to their respective physicochemical characteristics and their respective ability to really generate ROS over-production in the mouse lungs. Despite the early activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) cell signaling pathway by AW and, in a lesser degree, SS PM2.5, in the murine lungs after acute and sub-chronic exposures, the critical redox homeostasis was not restored, even after the exposure cessation. Accordingly, an inflammatory response was reported through the activation of the nuclear factor-kappa B (NF-κB) cell signaling pathway activation, the secretion of cytokines, and the recruitment of inflammatory cells, in the murine lungs after the acute and sub-chronic exposures to AW and, in a lesser extent, to SS PM2.5, which persisted after the recovery period. Taken together, these original results provided, for the first time, new relevant insights that air pollution-derived PM2.5, with relatively high intrinsic OPs, induced oxidative stress and inflammation, which persisted admittedly at a lower level in the lungs after the exposure cessation, thereby contributing to the occurrence of molecular and cellular adverse events leading to the development and/or exacerbation of future chronic inflammatory lung diseases and even cancers.
Oxidative stress and inflammation induced by air pollution-derived PM2.5 persist in the lungs of mice after cessation of their sub-chronic exposure
https://orcid.org/0009-0008-9768-378X
https://orcid.org/0009-0001-9186-0764
https://orcid.org/0000-0001-5572-0871
https://orcid.org/0000-0002-5179-1311
Graphical abstract Display Omitted
Highlights Outdoor air PM2.5 had intrinsic OP related to their physico-chemical characteristics. Intrinsic OP of outdoor air PM2.5 predicted induction of oxidative stress in lungs. Nrf2 and NFκB cell signaling pathways were activated by outdoor air PM2.5 in lungs. Oxidative and inflammatory effects persisted in lungs despite exposure cessation. Better knowledge of the persistence of outdoor air PM2.5-induced lung toxicity.
Abstract More than 7 million early deaths/year are attributable to air pollution. Current health concerns are especially focused on air pollution-derived particulate matter (PM). Although oxidative stress-induced airway inflammation is one of the main adverse outcome pathways triggered by air pollution-derived PM, the persistence of both these underlying mechanisms, even after exposure cessation, remained poorly studied. In this study, A/JOlaHsd mice were also exposed acutely (24 h) or sub-chronically (4 weeks), with or without a recovery period (12 weeks), to two urban PM2.5 samples collected during contrasting seasons (i.e., autumn/winter, AW or spring/summer, SS). The distinct intrinsic oxidative potentials (OPs) of AW and SS PM2.5, as evaluated in acellular conditions, were closely related to their respective physicochemical characteristics and their respective ability to really generate ROS over-production in the mouse lungs. Despite the early activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) cell signaling pathway by AW and, in a lesser degree, SS PM2.5, in the murine lungs after acute and sub-chronic exposures, the critical redox homeostasis was not restored, even after the exposure cessation. Accordingly, an inflammatory response was reported through the activation of the nuclear factor-kappa B (NF-κB) cell signaling pathway activation, the secretion of cytokines, and the recruitment of inflammatory cells, in the murine lungs after the acute and sub-chronic exposures to AW and, in a lesser extent, to SS PM2.5, which persisted after the recovery period. Taken together, these original results provided, for the first time, new relevant insights that air pollution-derived PM2.5, with relatively high intrinsic OPs, induced oxidative stress and inflammation, which persisted admittedly at a lower level in the lungs after the exposure cessation, thereby contributing to the occurrence of molecular and cellular adverse events leading to the development and/or exacerbation of future chronic inflammatory lung diseases and even cancers.
Oxidative stress and inflammation induced by air pollution-derived PM2.5 persist in the lungs of mice after cessation of their sub-chronic exposure
https://orcid.org/0009-0008-9768-378X
https://orcid.org/0009-0001-9186-0764
https://orcid.org/0000-0001-5572-0871
https://orcid.org/0000-0002-5179-1311
Graphical abstract Display Omitted
Highlights Outdoor air PM2.5 had intrinsic OP related to their physico-chemical characteristics. Intrinsic OP of outdoor air PM2.5 predicted induction of oxidative stress in lungs. Nrf2 and NFκB cell signaling pathways were activated by outdoor air PM2.5 in lungs. Oxidative and inflammatory effects persisted in lungs despite exposure cessation. Better knowledge of the persistence of outdoor air PM2.5-induced lung toxicity.
Abstract More than 7 million early deaths/year are attributable to air pollution. Current health concerns are especially focused on air pollution-derived particulate matter (PM). Although oxidative stress-induced airway inflammation is one of the main adverse outcome pathways triggered by air pollution-derived PM, the persistence of both these underlying mechanisms, even after exposure cessation, remained poorly studied. In this study, A/JOlaHsd mice were also exposed acutely (24 h) or sub-chronically (4 weeks), with or without a recovery period (12 weeks), to two urban PM2.5 samples collected during contrasting seasons (i.e., autumn/winter, AW or spring/summer, SS). The distinct intrinsic oxidative potentials (OPs) of AW and SS PM2.5, as evaluated in acellular conditions, were closely related to their respective physicochemical characteristics and their respective ability to really generate ROS over-production in the mouse lungs. Despite the early activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) cell signaling pathway by AW and, in a lesser degree, SS PM2.5, in the murine lungs after acute and sub-chronic exposures, the critical redox homeostasis was not restored, even after the exposure cessation. Accordingly, an inflammatory response was reported through the activation of the nuclear factor-kappa B (NF-κB) cell signaling pathway activation, the secretion of cytokines, and the recruitment of inflammatory cells, in the murine lungs after the acute and sub-chronic exposures to AW and, in a lesser extent, to SS PM2.5, which persisted after the recovery period. Taken together, these original results provided, for the first time, new relevant insights that air pollution-derived PM2.5, with relatively high intrinsic OPs, induced oxidative stress and inflammation, which persisted admittedly at a lower level in the lungs after the exposure cessation, thereby contributing to the occurrence of molecular and cellular adverse events leading to the development and/or exacerbation of future chronic inflammatory lung diseases and even cancers.
Oxidative stress and inflammation induced by air pollution-derived PM2.5 persist in the lungs of mice after cessation of their sub-chronic exposure
Barbier, Emeline (Autor:in) / Carpentier, Jessica (Autor:in) / Simonin, Ophélie (Autor:in) / Gosset, Pierre (Autor:in) / Platel, Anne (Autor:in) / Happillon, Mélanie (Autor:in) / Alleman, Laurent Y. (Autor:in) / Perdrix, Esperanza (Autor:in) / Riffault, Véronique (Autor:in) / Chassat, Thierry (Autor:in)
03.10.2023
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
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