Observation of inflammation and macrophage polarization in an experimental model of cigarette smoke-exposed mice and cigarette smoke extract (CSE)-induced RAW264.7 cells: An experimental preclinical study

INTRODUCTION: and in vitro COPD-related models. METHODS: cigarette smoke extract (CSE)-induced RAW264.7 macrophage model (10% CSE for 24 hours). Macrophage M1/M2 polarization and inflammatory responses were assessed using ELISA, qRT-PCR, immunohistochemistry, Western blotting, and flow cytometry. RESULTS: O/(mL/s), p<0.01). Histological examination revealed thickened bronchial walls, disrupted alveolar structure, and inflammatory cell infiltration. TNF-α (BALF: 290.6 ± 7.58 vs 125.6 ± 5.30 pg/mL, p<0.0001), IL-6 (BALF: 67.92 ± 3.02 vs 44.42 ± 2.62 pg/mL, p<0.001), and IL-1β (BALF: 120.3 ± 8.24 vs 87.52 ± 3.40 pg/mL, p<0.01) levels increased dramatically in both CS-exposed mice and CSE-induced RAW264.7 cells, whereas IL-10 levels decreased (BALF: 46.12 ± 1.71 vs 77.19 ± 3.96 pg/mL, p<0.001). CONCLUSIONS: CS and CSE exposure induced M1 macrophage polarization in mice, as well as 10% CSE-induced RAW 264.7 cells, which may be related to the activation of the NF-κB/NLRP3 signaling pathway.