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(Circulation Research. 2003;92:e78.)
© 2003 American Heart Association, Inc.

Letter to the Editor

Egr-1, a Major Link Between Infection and Atherosclerosis?

Jan Rupp, Matthias Maass

Institute of Medical Microbiology, and Hygiene, University of Lübeck, Lübeck, Germany, maass@hygiene.mu-luebeck.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

The study of Bea et al,¹ recently published in Circulation Research, investigated the role of Chlamydia pneumoniae infection in mouse macrophages on the induction of tissue factor (TF) via activation of Egr-1. Chlamydial infection of RAW mouse macrophages clearly resulted in enhanced Egr-1 protein expression and a subsequent time-dependent increase in TF mRNA expression and procoagulatory activity. We can confirm the postinfectious Egr-1 induction described by Bea et al. In addition, we can expand their findings and demonstrate a broader regulatory influence of Egr-1 on proatherosclerotic factors in C pneumoniae–infected mononuclear cells that is not limited to prothrombotic molecules and not restricted to mouse macrophages.

We performed similar experiments as Bea et al¹ but used blood monocytes from healthy blood donors and found that infection with the cardiovascular chlamydial strain CV-6 (isolated from a 68-year-old man with coronary restenosis²) significantly induced Egr-1 mRNA expression (15.8-fold±4.7, n=5; P<0.01; RT-PCR, LightCycler, Roche Molecular Biochemicals) after 1 hour. This is in line with the results of Bea et al, who observed maximum Egr-1 protein levels in the nuclei of infected RAW cells at 1 to 2 hours after infection. In contrast to Bea et al who focused on TF expression in mouse macrophages, we were interested whether Egr-1 is involved in the regulation of C pneumoniae–induced expression of the vascular endothelial growth factor (VEGF), which has been recently incriminated to promote atherosclerotic lesion formation and thus might also link infection and atherosclerosis.³ Enhanced VEGF immunoreactivity . . . [Full Text of this Article]