The Journal of allergy and clinical immunology · 2025
Traffic-emitted ultrafine particles disrupt macrophage efferocytosis and resolution of allergic lung inflammation.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Brüggemann Thayse R, Tavares Luciana P, Almanzar Nicole, Singh Dilpreet, Batchelder Holly, Nshimiyimana Robert, Haber Adam L, Demokritou Philip, Serhan Charles N, Levy Bruce D
Аннотация
BACKGROUND: 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.
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.