Clinical evidence has shown an elevated
myocardial infarction (MI) risk after PM2.5 (particulate matter < 2.5 μm) exposure. Incident MI may result from
rupture of vulnerable plaques. To test whether PM2.5 could promote plaque vulnerability, we exposed PM2.5 to
apoe-/- mice by intranasal instillation. We detected the
lipid,
collagen, macrophage and smooth muscle cells (SMCs) content, and fibrous cap thickness to evaluate the plaque vulnerability. Plaques in HFD-fed mice with PM2.5 treatment for 24 weeks had increased
lipid content and macrophage recruitment, and reduced
collagen content, fibrous cap thickness and SMCs infiltration. Besides, 4-week exposure to PM2.5 could reduce the fibrous cap thickness,
collagen content, but increase the macrophage infiltration and SMCs loss in a rapid
atherosclerosis model. In existing plaques, PM2.5 could also decrease the fibrous cap thickness,
collagen content. In RAW264.7, PM2.5 could promote the transformation of macrophage into foam cells. The expression of TLR4/MyD88/NFκB and CD36 were upregulated by PM2.5 treatment. Besides, the expression of CD36 promoted by PM2.5 was downregulated by the TLR4 inhibitor or MyD88/NFκB
SiRNA. In conclusion, our data indicated that short- and long-term PM2.5 exposure increased plaque vulnerability. The underlying mechanism might be the PM2.5-enhanced formation of foam cells via TLR4/MyD88/NFκB pathway.