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April 13, 2026Particle and Fibre Toxicology2 citationsOpen Access

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

KMKirsty MeldrumAKAyokulehin M. KosokoMLMartin Oliver Leonard

Key Points

  • This research aims to understand how pollutant particles, particularly diesel exhaust particles, exacerbate type 2 inflammation linked to house dust mites during allergic asthma.
  • Used mouse models with intranasal exposure to diesel exhaust particles and house-dust-mite.
  • Conducted bulk transcriptomics and single-cell proteomic profiling to analyze inflammatory responses.
  • Assessed chemokine levels and macrophage recruitment in response to pollutants.
  • Performed trajectory analysis to track monocyte-derived macrophage populations.
  • Diesel exhaust particles combined with house dust mites significantly increased type 2 inflammatory markers and eosinophilia.
  • Identified a specific subset of macrophages (Cd11c⁺, Gpnmb⁺) that expanded in response to pollutant exposure.
  • High-content imaging confirmed increased macrophage numbers and chemokine production in the airways.
  • Similar transcriptomic responses were observed with different pollutant particles, indicating a shared mechanism.

Abstract

Abstract 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 In mice subjected to repeated intranasal exposures, DEP alone had modest effects, whereas DEP + HDM markedly increased type-2 inflammatory indicators (Serum IgE; Airway Il13, Il4 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.

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Cite This Study

Meldrum et al. (2026) studied this question.

synapsesocial.com/papers/69dc887f3afacbeac03ea506https://doi.org/10.1186/s12989-026-00675-8
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