Chronic exposure to biomass ambient particulate matter triggers alveolar macrophage polarization and activation in the rat lung.

The role of alveolar macrophages (AMs) in chronic obstructive pulmonary disease is unclear. We characterized the function of AMs in rats chronically exposed to biomass fuel smoke (BMF) and studied the signal pathways that regulate AMs polarization. One hundred and eighty male Sprague-Dawley rats were divided into BMF group and clean air control (CON) group. After BMF smoke exposure for 4 days, 1 month and 6 months, the cytokine secretion and function of AMs were determined by flow cytometry, quantitative polymerase chain reaction, Western blotting and immunofluorescence. Bone marrow-derived macrophages were cultured and exposed to particulate matter (PM) from the smoke. Exposure initially promoted pro-inflammatory factors, but pro-inflammatory macrophages shared features of anti-inflammatory macrophages. Consistent with IL-4 upregulated in bronchoalveolar lavage fluid, p-Stat6 and peroxisome proliferator-activated receptor γ (PPARγ) in AMs elevated at 4 days of exposure. After 6 months of exposure, CD206, TGF-β1 and p-Smad3 were significantly higher than the control groups. PPARγ reversed the M1 phenotype induced by PM in vitro and drove the macrophages into the M2 phenotype. Altogether, the study demonstrates the dynamic phenotype and functional changes in AMs during exposure to BMF smoke.