Effects of Particulate Matter 10 Inhalation on Lung Tissue RNA expression in a Murine Model

BACKGROUND: Particulate matter 10 (PM(10); airborne particles <10 μm) inhalation has been demonstrated to induce airway and lung diseases. In this study, we investigate the effects of PM(10) inhalation on RNA expression in lung tissues using a murine model. METHODS: Female BALB/c mice were affected with PM(10), ovalbumin (OVA), or both OVA and PM(10). PM(10) was administered intranasally while OVA was both intraperitoneally injected and intranasally administered. Treatments occurred 4 times over a 2-week period. Two days after the final challenges, mice were sacrificed. Full RNA sequencing using lung homogenates was conducted. RESULTS: While PM(10) did not induce cell proliferation in bronchoalveolar fluid or lead to airway hyper-responsiveness, it did cause airway inflammation and lung fibrosis. Levels of interleukin 1β, tumor necrosis factor-α, and transforming growth factor-β in lung homogenates were significantly elevated in the PM(10)-treated group, compared to the control group. The PM(10) group also showed increased RNA expression of Rn45a, Snord22, Atp6v0c-ps2, Snora28, Snord15b, Snora70, and Mmp12. Generally, genes associated with RNA splicing, DNA repair, the inflammatory response, the immune response, cell death, and apoptotic processes were highly expressed in the PM(10)-treated group. The OVA/PM(10) treatment did not produce greater effects than OVA alone. However, the OVA/PM(10)-treated group did show increased RNA expression of Clca1, Snord22, Retnla, Prg2, Tff2, Atp6v0c-ps2, and Fcgbp when compared to the control groups. These genes are associated with RNA splicing, DNA repair, the inflammatory response, and the immune response. CONCLUSION: Inhalation of PM(10) extensively altered RNA expression while also inducing cellular inflammation, fibrosis, and increased inflammatory cytokines in this murine mouse model.