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Ozone Exposure Induces Anemia via Immune-Inflammatory Disruption of Erythroid Homeostasis

Year: 2025
Type: article
Abstract: High Resolution Image Download MS PowerPoint Slide Ground-level ozone (O 3 ), a major ambient air pollutant, is epidemiologically linked to anemia, but its mechanisms remain unclear. This study employed integrated phenotypic, histopathological, and transcriptomic analyses to explore the molecular mechanisms of O 3 -induced anemia. Male C57BL/6J mice underwent 28-day whole-body O 3 exposure at environmentally relevant concentrations (0.25 and 0.50 ppm, 4 h/day) alongside clean air controls. Significant hematological alterations occurred only at 0.50 ppm, including reduced erythroid parameters (red blood cells, hemoglobin, hematocrit, and reticulocytes) and systemic immune-inflammatory activation (increased lymphocyte count). This exposure level induced hematopoietic damage manifested as impaired progenitor cell differentiation (CFU-GEMM colony-forming capacity decreased by 20.55%, p < 0.05), reduced bone marrow hematopoietic cells, and extramedullary hematopoiesis in the spleen. Transcriptomic analysis identified 30 immune-inflammatory-related differentially expressed genes (IR-DEGs). Hierarchical network analysis integrating protein–protein interaction topology and transcriptional regulation revealed a core regulatory axis of transcription factors and 7 hub genes. Quantitative real-time PCR (qRT-PCR) and protein assays demonstrated that Jund is one of the key nodes in the regulatory network, which regulates critical immune-inflammatory genes (Ccl5, Lck, and Ifng). These findings indicate that Jund, as a key transcription factor in immune-inflammatory processes, mediates O 3 -induced disruption of erythrocyte homeostasis, thereby providing experimental evidence for environmental anemia prevention.
Institution: Shanxi University
Language: English
Open Access status: gold
Estimated APC paid: $3,500
OpenAlex ID: W4415148517
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Cites: 62
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