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Final Program


Final Program

Immunometabolism

Colchicine Attenuates Fine Particulate Matter-Induced Foam Cell Formation and Human Monocyte Activation

Tu171 - Colchicine Attenuates Fine Particulate Matter-induced Foam Cell Formation and Human Monocyte Activation

Tuesday, June 24, 2025
6:00pm - 7:30pm East Coast USA Time
Abstract Text:

Introduction: Exposure to air pollutant fine particulate matter (PM2.5) is an independent risk factor for cardiovascular diseases. PM2.5 can target monocytes and macrophages, disturb their mitochondrial metabolism, and trigger foam cell formation. PM2.5 also potentiates NLRP3 inflammasome activation and IL-1β release, implicated in atherosclerosis. Colchicine is the only FDA-approved anti-inflammatory drug for atherosclerosis. This agent attenuates granulocyte functions, phagocytosis, and NLRP3 inflammasome assembly, potentially modulating atherosclerotic lesions. This study tested the hypothesis that colchicine attenuates PM2.5-induced foam cell formation.

Methods: Primary human monocytes isolated from blood were seeded in RPMI medium, supplemented with 10%FBS, and exposed to PBS (Control) or NIST2786-PM2.5 at 100 µg/mL concentration, for 24 h with or without colchicine (5 ng/mL). Data are mean ± SD, and compared through One-way ANOVA, followed by Tukey.

Results: Colchicine attenuated PM2.5-stimulated reactive oxygen species generation (Ctrl:1.00±0.07; PM100:1.19±0.14*; PM100+Colc:1.16±0.11, *P=0.017 vs Ctrl) and phagocytosis (Ctrl:1.00±0.12; PM100:1.71±0.30*; PM100+Colc:1.47±0.25*/#, *P < 0.0001 vs Ctrl and # vs PM100). It also reduced lipid accumulation induced by PM2.5 (Ctrl:1.00±0.11; PM100:1.14±0.12*; PM100+Colc:1.00±0.12#, *P < 0.0001 vs Ctrl and # vs PM100), but these effects appeared independent of IL-1β, IL-6, TNF- and m-CSF, mediators whose production the pollutant enhances while IL-10 (Ctrl:1.30±0.31; PM100:731.8±40.70*; PM100+Colc:425.5±176.3*/#, *P < 0.0001 vs Ctrl and #vs PM100) and MCP-1 (Ctrl:118.7±9.27; PM100:2088.0±967.9*; PM100+Colc:1017.0±798.3, *P < 0.0001 vs Ctrl) levels fell with colchicine.

Conclusion: Colchicine attenuates foam cell formation and aspects of monocyte activation induced by acute exposure to PM2.5, likely in a manner independent of the NLRP3 inflammasome pathway.