Air pollution, particularly exposure to fine particulate matter (PM
2.5), poses a substantial risk to human health. Diesel exhaust particles (DEPs), a major constituent of PM
2.5, contain chemically reactive components that promote inflammation, oxidative stress, and immune dysfunction. Although the
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Air pollution, particularly exposure to fine particulate matter (PM
2.5), poses a substantial risk to human health. Diesel exhaust particles (DEPs), a major constituent of PM
2.5, contain chemically reactive components that promote inflammation, oxidative stress, and immune dysfunction. Although the acute toxicity of PM
2.5 and DEPs has been extensively studied, their effects under “sub-toxic” conditions—defined here as exposures that do not cause measurable cytotoxicity based on LDH release but still impair cellular function—remain poorly understood. This study investigated the impact of low-toxicity exposure to DEPs and PM
2.5 on dendritic cell (DC) function using the human plasmacytoid DC-like cell line PMDC05. Cells exposed to DEPs or PM
2.5 exhibited minimal cytotoxicity but accumulated intracellular particles, resulting in impaired endocytosis, phagocytosis, and interferon gene expression upon TLR7 stimulation. These functional impairments were not observed following TLR4 stimulation, suggesting a selective disruption of endolysosomal signalling. The findings demonstrate that DEPs and PM
2.5 can impair innate immune responses without inducing cell death, likely through lysosomal overload and altered intracellular trafficking. This study identifies a non-cytotoxic pathway through which particulate air pollution may compromise antiviral immunity, thereby increasing susceptibility to infection in polluted environments. Strategies aimed at preserving lysosomal integrity and dendritic cell function may help mitigate the immunotoxic effects of airborne particles.
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