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Polystyrene nanoplastics reprogramed pulmonary metabolisms mediated by immune regulation of myeloid hypoxia-inducible factor 1α
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Researchers exposed mice to polystyrene nanoplastics through their lungs for six weeks and found the particles triggered lung inflammation, scarring, and a metabolic switch to glycolysis — the same energy-burning pattern seen in activated immune cells during injury. A key protein called HIF-1α in immune cells was identified as the driver of these metabolic changes, offering a potential target for understanding nanoplastic lung toxicity.
Exposure to nanoplastics (NPs), a pervasive environmental pollutant, presents potential health risks. Pulmonary exposure to NPs has been shown to disrupt both pulmonary metabolic status and immune homeostasis, leading to concerns about their impact on respiratory health and systemic well-being. However, the underlying linkage and mechanisms remain elusive. Following intratracheal instillation of polystyrene nanoplastics (PS-NPs) (5 μg/day for six weeks) in C57BL/6 mice, a combined approach of flow cytometry and metabolome analysis was applied to elucidate the interplay between metabolic and immune responses. Histopathological analysis indicated adverse lung effects from PS-NP exposure, characterized by immune cell infiltration and fibrosis. Flow cytometry analysis of lung immune cells further showed increased Ly6Clow monocyte and decreased neutrophil proportions. Metabolome analysis of the lungs of PS-NP-exposed mice revealed a metabolic shift with activated glycolysis and biosynthetic pathways. Such metabolic changes were consistent with hypoxia-inducible factor 1α (HIF-1α)-mediated upregulation of glycolysis, a metabolic phenotype commonly mimicking that of the activated myeloid cells during inflammation. Real-time quantitative PCR demonstrated glycolysis activation in the lungs and confirmed HIF-1α activation in myeloid cells using an in vitro RAW 264.7 macrophage model. To further investigate the contribution of HIF-1α in myeloid cells in lung metabolism, a myeloid cell-specific HIF-1α-deficient (Lyz2cre Hif1af/f) mouse model was employed. A shortened 2-week exposure experiment confirmed the indispensable role of HIF-1α in myeloid cells for metabolic modulation during PS-NP exposure. Spearman correlation analysis identified associations between immune cell populations and HIF-1α-related metabolites, suggesting potential crosstalk between HIF-1α-mediated metabolic alterations and immune changes induced by PS-NPs. Our study reveals the critical role of HIF-1α in myeloid cells in modulating lung metabolism and its potential crosstalk with the immune system, offering novel insights on the progression of NP-induced pulmonary toxicity.
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