Pollutant particles enhance house dust mite induced type 2 inflammation and the recruitment of monocyte derived Cd11c+ Gpnmb+ macrophages to the airway lumen

BACKGROUND: Air pollution particles exacerbate allergic asthma and can enhance inflammatory responses to allergen exposure, but the cellular mechanisms involved remain incompletely defined. We examined how diesel exhaust particles (DEP) enhance house-dust-mite (HDM) inflammatory responses within the lung and characterised potential mechanisms that may contribute to enhanced type 2 (T2) inflammatory responses. RESULTS: Nanoparticles) in the same exposure model, revealed a shared luminal transcriptomic response and AAM/chemokine programme as with DEP. CONCLUSIONS: Our data suggests that pollutant particles such as DEP may contribute to enhanced HDM induced type 2 inflammation by expanding Ccr2-dependent monocyte-derived macrophages into the airway lumen and licensing a Th2-cytokine-responsive chemokine programme (Ccl8- Ccr8 to recruit Th2 cells; Ccl24-Ccr3 to recruit eosinophils). These findings identify luminal recruited macrophages as important targets in allergic inflammation within the lung, providing insight into potential mechanisms from which exposure and disease mitigation strategies may be developed.