ArticleBMC pulmonary medicine2026
Impact of particulate matter 2.5 on a mouse model of lung adenocarcinoma.
Article in BMC pulmonary medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOver the years, lung cancer incidence in never-smokers has been rising. Air pollution is a non-smoking-related factor that promotes lung cancer progression. Particulate matter 2.5 (PM2.5) is a component of air pollution that is associated with a type 2 immune response mediated by group 2 innate lymphoid cells (ILC2) and T helper 2 (Th2) cells. Furthermore, PM2.5 can activate fibroblasts, induce the secretion of collagen, and contribute to the development of lung fibrosis. Although type 2 immune response and lung fibrosis are described as pro-tumorigenic in lung cancer, whether PM2.5-driven type 2 immune response and/or lung fibrosis promote lung cancer tumorigenesis in mouse models of lung cancer remains unclear. This study investigated the impact of PM2.5 on the type 2 immune response, lung fibrosis, and lung cancer tumorigenesis in vivo.
methodsWe treated EGFR and KRAS/Trp53 mouse models of LUAD intranasally with PM2.5, analyzed lung tumor burden and lung fibrosis by histology, and changes in type 2 immune cell (ILC2, Th2) and CAF markers by flow cytometry. Different durations of PM2.5 treatment (3-week short-term vs. 6-week long-term), experimental time points (10 weeks vs. 15 weeks), and intervals between the onset of EGFR and KRAS/Trp53 mutations and first exposure to PM2.5 (3 days vs. 4 weeks delayed) were assessed. Unpaired t-test and One-way ANOVA statistical tests were utilized.
resultsWe found that PM2.5 did not significantly impact lung tumor burden in EGFR and KRAS/Trp53 mouse models of LUAD. Notably, PM2.5 did not significantly affect the type 2 immune response mediated by ILC2 and Th2 cells. However, long-term exposure to PM2.5 or delayed treatment with PM2.5 significantly increased the abundance of CD90.2+ CAFs in lung cancer without impacting lung cancer burden.
conclusionsIn summary, while PM2.5 did not significantly impact EGFR and KRAS/Trp53 lung tumor burden or the type 2 immune response, long-term or delayed exposure to PM2.5 promoted CD90.2+ CAFs in vivo. This study demonstrates that preclinical modeling of PM2.5-driven LUAD requires further validation and consideration of confounding variables to reflect air pollution-associated LUAD observed in humans.
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