¹The Hong Kong Polytechnic University, Rehabilitation Sciences, Hong Kong, Hong Kong, SAR of China

Background: Chronic Obstructive Pulmonary Disease (COPD) features chronic airway inflammation and is linked to elevated risks of anxiety and depression. While PM_2.5 is epidemiologically associated with COPD exacerbations, it remains unclear whether real-world ambient exposure aggravates pulmonary inflammation and triggers brain inflammatory changes relevant to mood disorders.

Aims & Objectives: To examine whether ambient PM_2.5 exposure augments inflammatory protein expression in the lung and hippocampus in COPD compared to control mice.

Method: Male and female C57BL/6 mice (6–8 weeks) were assigned to filtered air + control, filtered air + COPD, ambient air + control, or ambient air + COPD. COPD-like inflammation was induced by intratracheal LPS once a week for four weeks. Ambient exposure used a custom chamber drawing roadside traffic air continuously for 4 weeks; controls received filtered air in the same setup. One week after the last LPS instillation, lungs and hippocampi were collected for western blot of inflammatory markers.

Results: LPS robustly increased pulmonary IL-17A versus vehicle in male mice, validating COPD-like inflammation. Four-week ambient PM_2.5 did not significantly elevate IL-17A, IL-1β, IL-6, or NF-κB in lung or hippocampus in either control or COPD male mice compared with filtered air. No significant difference was observed between the LPS treatment and PM_2.5 exposure in the female lung. Thus, under these conditions, roadside PM_2.5 did not exacerbate pulmonary or hippocampal inflammatory protein signatures beyond LPS effects.

Discussion & Conclusions: In an LPS-induced COPD model, one month of real-world roadside PM_2.5 exposure did not worsen inflammatory markers in lung or hippocampus. Findings suggest that exposure duration/composition and disease state may critically gate PM_2.5 impact on lung–brain inflammation. Limitations include short exposure, variability in ambient PM_2.5 composition, reliance on LPS rather than smoke-induced COPD, and absence of behavioral readouts. Future work should extend exposure, include controlled PM_2.5 dosing and depression-relevant behaviors, and probe mechanistic pathways to define pollution–COPD–brain interactions.