Microplastic
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ABSTRACT:
PROVIDER: PRJNA1168257 | ENA |
REPOSITORIES: ENA
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Project description:Rationale Microplastics are a pressing global concern and inhalation of microplastic fibers has been associated with interstitial and bronchial inflammation in flock workers. However, how microplastic fibers affect the lungs is unknown. Objectives Our aim was to assess the effects of 12x31 µm nylon 6,6 (nylon) and 15x52 µm polyethylene terephthalate (polyester) textile microplastic fibers on lung epithelial growth and differentiation. Methods We used human and murine alveolar and airway-type organoids as well as air-liquid interface cultures derived from primary lung epithelial progenitor cells and incubated these with either nylon or polyester fibers or nylon leachate. In addition, mice received one dose of nylon fibers or nylon leachate and 7 days later organoid-forming capacity of isolated epithelial cells was investigated. Results We observed that nylon microfibers, more than polyester, inhibited developing airway organoids and not established ones. This effect was mediated by components leaching from nylon. Epithelial cells isolated from mice exposed to nylon fibers or leachate, also formed fewer airway organoids, suggesting long-lasting effects of nylon components on epithelial cells. Part of these effects were recapitulated in human air-liquid interface cultures. Transcriptome analysis revealed upregulation of Hoxa5 post-exposure to nylon fibers. Inhibiting Hoxa5 protein during nylon exposure restored airway organoid formation, confirming Hoxa5's pivotal role in the effects of nylon. Conclusions These results suggest that components leaching from nylon 6,6 may especially harm developing airways and/or airways undergoing repair and we strongly encourage to characterize both hazard of and exposure to microplastic fibers in more detail.
2023-12-31 | GSE238065 | GEO
Project description:Transcriptional profiling of the waterflea Daphnia magna, when exposed to microplastic particles made of polyvinylchloride (PVC) and the incorporated plasticizer diisononyl phtalate (DINP)
2025-12-18 | GSE84173 | GEO
Project description:Metagenome of microplastic in soil
| PRJNA819581 | ENA
Project description:Microplastic particles that occur in the environment are coated with different biomolecules forming an eco-corona on the particles' surface, which could consequently lead to a specific interaction of the constituents of the eco-corona with membrane receptors. To date, it is not fully understood how strong microplastic particles with and without an eco-corona bind to cellular membranes and which underlying mechanisms are responsible for cellular internalization. Here we analyzed the protein composition of two different eco-coronas (freshwater and saltwater) by LC-MS/MS.
2025-03-07 | PXD050078 | Pride
Project description:Wastewater microplastic microbiome characterization
| PRJNA638613 | ENA
Project description:Marine microplastic polluted sediment metagenome Raw sequence reads
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Project description:Microplastic-contaminated soil Raw sequence reads
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Project description:Freshwater Microplastic eDNA Raw sequence reads
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Project description:Microplastics are increasingly detected in the atmosphere and human tissues, yet their long-term effects on lung biology remain unclear. Here, we identified multiple microplastic polymers in human lung tissues using pyrolysis–gas chromatography/mass spectrometry (Py-GC/MS). Using a chronic inhalation model with environmentally relevant concentrations, we show that microplastic exposure induces progressive pulmonary fibrosis in a particle size–dependent manner, with nanoscale particles producing stronger fibrogenic effects than micron-scale particles. Single-cell transcriptomics revealed expansion of Fabp5⁺ interstitial macrophages and early fibroblast activation specifically following nanoscale exposure. Cell–cell communication analysis identified PDGFA–PDGFRA signaling as a key mediator of macrophage–fibroblast interactions. Mechanistically, nanoscale microplastics activated a Fabp5–FOXK2–PDGFA transcriptional axis in macrophages, whereas micron-scale particles showed minimal activation. Fabp5 silencing suppressed this pathway and attenuated pulmonary fibrosis, revealing a macrophage-driven mechanism linking inhaled microplastics to fibrotic lung remodeling.
2026-03-16 | GSE324602 | GEO