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Article Abstract
The effect of atmospheric ultrafine particulate matter (UPM) on respiratory allergic diseases has been investigated for decades; however, the precise molecular mechanisms underlying these effects remain poorly understood. In this study, we used a simulated UPM (sUPM) generated via the spark discharge method to refine black carbon, a core particle that closely mimics real-world UPM, including the size (i.e., size of agglomerates: 165 nm) and organic carbon/elemental carbon ratio (i.e., 2.62). When 25 μg/mouse of dispersed sUPM was instilled into the lungs of mice, it promoted the infiltration and degranulation response of pulmonary mast cells, and exposure to sUPM in an immunoglobulin E (IgE)-mediated passive anaphylaxis model intensified the degranulation response of peripheral mast cells. These effects of sUPM were demonstrated to amplify the downstream signaling mechanism of the high-affinity IgE receptor (FcεRI) mediated by IgE when tested using rat basophil leukemia (RBL)-2H3 and mouse bone marrow-derived mast cells (BMMCs) collected from the bone marrow of BALB/c mice. These results indicate that airborne UPM can exacerbate type 1 hypersensitivity reactions by enhancing the IgE-mediated signaling pathways within mast cells. Furthermore, this study provided mechanistic evidence on exacerbated allergic pulmonary diseases induced by UPM inhalation.
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| http://dx.doi.org/10.1016/j.jhazmat.2024.136705 | DOI Listing |
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