To the Editor: In their Preliminary Communication, Dr Sun and colleagues1 showed that in apolipoprotein E knockout mice, exposure to concentrated ambient particles potentiated atherosclerosis under a condition of a high-fat diet. These observations suggest a Trojan horse hypothesis that could explain involvement of microparticles in atherogenesis.
Circulating lipid particles could serve as “lipid bullets” carrying lipophilic components or microspheric compounds such as airborne particles. These particles might infiltrate the intima, leading to enhanced plaque formation by inducing macrophage-mediated cytokine production and foam cell formation. Circulating lipoprotein particles (eg, apolipoprotein B [apo-B]-containing particles in the human postprandial state) loaded with lipophilic microparticles have been shown to transit endothelium and accumulate in the subendothelial matrix with subsequent engulfment by local macrophages.2 - 3
In contrast with “naked” apo-B–containing particles, which offer cholesterol to macrophages to maintain their functional structure, apo-B–containing lipoprotein particles loaded with lipophilic compounds, such as the inhaled 2.5-μm airborne particles in Sun et al, may disturb intracellular processes in subendothelial residing macrophages. Disruption of cellular metabolism inhibits prevention of apoptosis and activates proinflammatory pathways,4 factors that are present in an atherosclerotic lesion.5 - 6 A reduction of these loaded lipoprotein particles by statin therapy could additionally limit its biological activity (pleiotropic effects of statins).
In considering this hypothesis, it would be helpful if the authors could analyze the level of airborne particles in specific lipoprotein fractions and assess whether airborne particles are located in subendothelial macrophages.
Financial Disclosures: None reported.
Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature
Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal
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