Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release
Desert dust is increasingly recognized as a major air pollutant affecting respiratory health. Since desert dust exposure cannot be regulated, the hazardousness of its components must be understood to enable health risk mitigation strategies. Saharan dust (SD) comprises about half of the global deser...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-02-01
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| Series: | Environment International |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0160412023000053 |
| _version_ | 1797903506800115712 |
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| author | Gerrit Bredeck Mathias Busch Andrea Rossi Burkhard Stahlmecke Khanneh Wadinga Fomba Hartmut Herrmann Roel P.F. Schins |
| author_facet | Gerrit Bredeck Mathias Busch Andrea Rossi Burkhard Stahlmecke Khanneh Wadinga Fomba Hartmut Herrmann Roel P.F. Schins |
| author_sort | Gerrit Bredeck |
| collection | DOAJ |
| description | Desert dust is increasingly recognized as a major air pollutant affecting respiratory health. Since desert dust exposure cannot be regulated, the hazardousness of its components must be understood to enable health risk mitigation strategies. Saharan dust (SD) comprises about half of the global desert dust and contains quartz, a toxic mineral dust that is known to cause severe lung diseases via oxidative stress and activation of the NLRP3 inflammasome-interleukin-1β pathway. We aimed to assess the physicochemical and microbial characteristics of SD responsible for toxic effects. Also, we studied the oxidative and pro-inflammatory potential of SD in alveolar epithelial cells and the activation of the NLRP3 inflammasome in macrophage-like cells in comparison to quartz dusts and synthetic amorphous silica (SAS).Characterization revealed that SD contained Fe, Al, trace metals, sulfate, diatomaceous earth, and endotoxin and had the capacity to generate hydroxyl radicals. We exposed A549 lung epithelial cells and wild-type and NLRP3-/- THP-1 macrophage-like cells to SD, three well-investigated quartz dusts, and SAS. SD induced oxidative stress in A549 cells after 24 h more potently than the quartz dusts. The quartz dusts and SAS upregulated interleukin 8 expression after 4 h and 24 h while SD only caused a transient upregulation. SD, the quartz dusts, and SAS induced interleukin-1β release from wild-type THP-1 cells>20-fold stronger than from NLRP3-/- THP-1 cells. Interleukin-1β release was lower for SD, in which microbial components including endotoxin were heat-destructed.In conclusion, microbial components in SD are pivotal for its toxicity. In the epithelium, the effects of SD contrasted with crystalline and amorphous silica in terms of potency and persistence. In macrophages, the strong involvement of the NLRP3 inflammasome emphasizes the acute and chronic health risks associated with desert dust exposure. |
| first_indexed | 2024-04-10T09:35:12Z |
| format | Article |
| id | doaj.art-45a528ce3ac54d5984ae7aea75cc6e65 |
| institution | Directory Open Access Journal |
| issn | 0160-4120 |
| language | English |
| last_indexed | 2024-04-10T09:35:12Z |
| publishDate | 2023-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Environment International |
| spelling | doaj.art-45a528ce3ac54d5984ae7aea75cc6e652023-02-18T04:16:10ZengElsevierEnvironment International0160-41202023-02-01172107732Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine releaseGerrit Bredeck0Mathias Busch1Andrea Rossi2Burkhard Stahlmecke3Khanneh Wadinga Fomba4Hartmut Herrmann5Roel P.F. Schins6IUF – Leibniz Research Institute for Environmental Medicine, Düsseldorf, GermanyIUF – Leibniz Research Institute for Environmental Medicine, Düsseldorf, GermanyIUF – Leibniz Research Institute for Environmental Medicine, Düsseldorf, GermanyInstitute for Energy and Environmental Technology e.V. (IUTA), Duisburg, GermanyAtmospheric Chemistry Department (ACD), Leibniz-Institute for Tropospheric Research (TROPOS), Leipzig, GermanyAtmospheric Chemistry Department (ACD), Leibniz-Institute for Tropospheric Research (TROPOS), Leipzig, GermanyIUF – Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany; Corresponding author at: IUF - Leibniz Research Institute for Environmental Medicine, Auf’m Hennekamp 50, 40225 Düsseldorf, Germany.Desert dust is increasingly recognized as a major air pollutant affecting respiratory health. Since desert dust exposure cannot be regulated, the hazardousness of its components must be understood to enable health risk mitigation strategies. Saharan dust (SD) comprises about half of the global desert dust and contains quartz, a toxic mineral dust that is known to cause severe lung diseases via oxidative stress and activation of the NLRP3 inflammasome-interleukin-1β pathway. We aimed to assess the physicochemical and microbial characteristics of SD responsible for toxic effects. Also, we studied the oxidative and pro-inflammatory potential of SD in alveolar epithelial cells and the activation of the NLRP3 inflammasome in macrophage-like cells in comparison to quartz dusts and synthetic amorphous silica (SAS).Characterization revealed that SD contained Fe, Al, trace metals, sulfate, diatomaceous earth, and endotoxin and had the capacity to generate hydroxyl radicals. We exposed A549 lung epithelial cells and wild-type and NLRP3-/- THP-1 macrophage-like cells to SD, three well-investigated quartz dusts, and SAS. SD induced oxidative stress in A549 cells after 24 h more potently than the quartz dusts. The quartz dusts and SAS upregulated interleukin 8 expression after 4 h and 24 h while SD only caused a transient upregulation. SD, the quartz dusts, and SAS induced interleukin-1β release from wild-type THP-1 cells>20-fold stronger than from NLRP3-/- THP-1 cells. Interleukin-1β release was lower for SD, in which microbial components including endotoxin were heat-destructed.In conclusion, microbial components in SD are pivotal for its toxicity. In the epithelium, the effects of SD contrasted with crystalline and amorphous silica in terms of potency and persistence. In macrophages, the strong involvement of the NLRP3 inflammasome emphasizes the acute and chronic health risks associated with desert dust exposure.http://www.sciencedirect.com/science/article/pii/S0160412023000053African dustHazardLung inflammationAlveolar epitheliumLung diseaseCrystalline silica |
| spellingShingle | Gerrit Bredeck Mathias Busch Andrea Rossi Burkhard Stahlmecke Khanneh Wadinga Fomba Hartmut Herrmann Roel P.F. Schins Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release Environment International African dust Hazard Lung inflammation Alveolar epithelium Lung disease Crystalline silica |
| title | Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release |
| title_full | Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release |
| title_fullStr | Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release |
| title_full_unstemmed | Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release |
| title_short | Inhalable Saharan dust induces oxidative stress, NLRP3 inflammasome activation, and inflammatory cytokine release |
| title_sort | inhalable saharan dust induces oxidative stress nlrp3 inflammasome activation and inflammatory cytokine release |
| topic | African dust Hazard Lung inflammation Alveolar epithelium Lung disease Crystalline silica |
| url | http://www.sciencedirect.com/science/article/pii/S0160412023000053 |
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