Acute co-exposure to urban particulate matter and aircraft noise elicits lung-centered immune-redox proteomic remodeling in mice.

Authors

Corrado Ameli, Bharath Anila Bhuvanendran Nair, Amalie Schufri Klinkby, Marin Kuntic, Matthias Oelze, Ivana Kuntic, Elle Wilson, Omar Hahad, Alex von Kriegsheim, Thomas Münzel, Reka Toth, Andreas Daiber, Petr V Nazarov, Adelina Rogowska-Wrzesinska

Published in

Environmental pollution (Barking, Essex : 1987). Pages 129165. Sep 24, 2026. Epub Sep 24, 2026.

Abstract

Particulate air pollution and transportation noise frequently co-occur, but their combined molecular effects are poorly defined. We used data-independent acquisition (DIA) LC-MS/MS proteomics to profile lung, brain, and heart from male C57BL/6J mice exposed for 3 days to NIST SRM 1648a urban particulate matter (PM), aircraft noise (NOISE), PM + NOISE, or control conditions. The exposure model is the acute co-exposure paradigm previously characterised with orthogonal functional, redox, and inflammatory endpoints by Kuntic et al. The lung was the dominant responsive organ. PM + NOISE produced the broadest pulmonary response and the strongest induction of immune and macrophage-associated proteins, including acute-phase, particle-handling, interferon-linked, and phagosome-associated markers. This immune signal was accompanied by NADPH oxidase and iron-handling components, altered epithelial barrier markers, and endothelial and extracellular-matrix perturbation. The principal pulmonary modules agreed with orthogonal endpoints previously measured in the parent exposure experiment, including pulmonary NOX-2 and HO-1 protein, in situ reactive oxygen species formation, Cd68 and Mcp-1 transcripts, circulating cytokines, increased systolic blood pressure, impaired endothelium-dependent relaxation of the aorta, and cerebral and retinal arteriolar microvascular dysfunction. Brain and heart responses were lower in amplitude and involved selective redox, neuronal, contractile, metabolic and matrix-associated programs. Observed-versus-expected analyses showed that most stress-responsive proteins scaled proportionally, whereas a smaller set enriched for ribosome, RNA-processing, and chromatin functions was constrained. Integration with transcriptomic data showed strong mRNA-protein concordance in lung and greater transcript-protein divergence in brain and heart. Acute co-exposure therefore increases early pulmonary immune-redox burden without uniform additive escalation across molecular systems.

PMID:
42785619
Bibliographic data and abstract were imported from PubMed on 25 Sep 2026.

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