biostudies-otherUnknown157Robert NshimiyimanaMus musculus (mouse)https://www.ebi.ac.uk/biostudies/studies/S-BSST2110biostudies-otherRobert NshimiyimanaCharles N. SerhanfalseTraffic-emitted ultrafine particles disrupt macrophage efferocytosis and resolution of allergic lung inflammationBackground: Particulate matter (PM) in air pollution is a major health concern. PM includes ultrafine particles (UFPs; PM0.1 and particles of < _0.1 𝛍m), which can evoke lung inflammation. However, the impact of UFPs on the resolution of lung inflammation, a potentially important link to chronic inflammatory diseases, remains to be determined. Objective: We sought to investigate the impact of UFPs on the resolution of allergic lung inflammation and to identify potential therapeutic interventions to mitigate these effects. Methods: UFPs were collected from urban Boston. Using a mouse model, transient allergic lung inflammation was induced by exposure to house dust mite. Mice were then exposed to UFPs, and their inflammatory responses were assessed. The therapeutic potential of a resolution agonist, resolvin D2 (RvD2; 7S,16R,17S-trihydroxy-4Z,8E,10Z,12E,14E,19Z- docosahexaenoic acid), was also determined. Results: UFP exposure impaired lung eosinophil clearance and reduced macrophage efferocytosis, key processes in resolving lung inflammation. This disruption was mediated by altered expression of ecto-5΄-nucleotidase (Nt5e, gene encoding for CD73). Administration of RvD2, a potent proresolving mediator, increased macrophage efferocytosis of apoptotic eosinophils and neutrophils and partially corrected the UFP-disrupted resolution mechanisms. Conclusions: Environmental exposure to traffic-emitted UFPs can fundamentally undermine endogenous resolution processes —pathologic mechanisms that can be partially rescued by signaling pathways activated by RvD2. (J Allergy Clin Immunol 2026;157:238-52.)2025-09-30T00:00:00Z2026-05-27T15:30:26.611Z2025-06-24T17:55:46.832ZS-BSST2110