Fine particulate matter (PM2.5) air pollution poses a major risk to human health worldwide, and absorbed chemicals play a key role in determining the toxicity of PM2.5. After inhalation and entry into the lungs, PM2.5 components induce pro-inflammatory cytokines (e.g., interleukin (IL)-1β) in pulmonary cells. To test whether PM2.5 components induce IL-1β through signing pathways that include the toll-like receptor 4 (TLR4)/nuclear factor-κ-gene binding (NF-κB), nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3), we exposed the mouse macrophage cell-line RAW264.7 to both water and organic extracts of PM2.5 sampled over a 1-year period in Beijing, China. Varying degrees of oxidative stress and inflammatory responses were induced following exposure, while organic extracts of PM2.5 collected during the heating season induced more significant responses. This response is attributed to high concentrations of polycyclic aromatic hydrocarbons (PAHs) originating from coal combustion and biomass burning for domestic heating. The inhibition of signaling molecules suggested that increased IL-1β was associated with the TLR4/NF-κB pathway and NLRP3 inflammasome activation, with a slightly difference between water and organic extracts exposure groups, which was likely the result of different chemical components. Our study elucidated a potentially important mechanism by which PM2.5 components could trigger pulmonary inflammation, thus improving our understanding of the deleterious effects of this important and prevalent form of air pollution.
Keywords: IL-1β; Macrophage; NF-κB; NLRP3 inflammasome; PM(2.5) extracts.
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