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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 . . . [Full Text of this Article]

Marcel Twickler, MD, PhD
t.twickler@endo.umcn.nl
Department of Endocrinology
Radboud University Nijmegen Medical Centre
Nijmegen, the Netherlands

Geesje Dallinga-Thie, PhD
Department of Vascular Medicine
Erasmus University Medical Centre
Rotterdam, the Netherlands

Maarten-Jan Cramer, MD, PhD
Department of Cardiology
University Medical Centre Utrecht
Utrecht, the Netherlands

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