The Journal of Experimental Medicine
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Published online January 7, 2008
doi:10.1084/jem.20070201
The Journal of Experimental Medicine, Vol. 205, No. 1, 19-24
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Qiu et al.
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BRIEF DEFINITIVE REPORT

 Human CMV infection induces 5-lipoxygenase expression and leukotriene B4 production in vascular smooth muscle cells

Hong Qiu1, Klas Strååt2, Afsar Rahbar2, Min Wan1, Cecilia Söderberg-Nauclér2, and Jesper Z. Haeggström1

1 Department of Medical Biochemistry and Biophysics, Division of Chemistry II, Karolinska Institutet, S-171 77 Stockholm, Sweden
2 Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, SE 171 76 Stockholm, Sweden

CORRESPONDENCE Cecilia Söderberg-Nauclér: Cecilia.Soderberg.Naucler{at}ki.se

Leukotrienes (LTs) are powerful proinflammatory lipid mediators that may play a central role in cardiovascular diseases, including arteriosclerosis, myocardial infarction, and stroke. Owing to restricted expression of 5-lipoxygenase (5-LO), the enzyme required for their synthesis, LTs are almost exclusively produced by myeloid cells. Here, we report that human cytomegalovirus (HCMV) infection of human vascular smooth muscle cells (SMCs) increases 5-LO mRNA levels by up to 170-fold in a dose- and time-dependent manner. Infected cells expressed 5-LO protein, as shown by immunohistochemistry, enabling them to synthesize bioactive LTB4. HCMV-infected vascular SMCs expressing 5-LO protein were readily detected in tissue samples from CMV-infected patients with inflammatory bowel disease or AIDS. Thus, pathogen-induced LT production in HCMV-infected tissues may contribute to local inflammation, consistent with the ability of HCMV to control cellular and immunological functions. HCMV-induced LT biosynthesis in SMCs offers a molecular mechanism to explain HCMV-induced pathogenesis in inflammatory diseases.

H. Qiu and K. Strååt contributed equally to this work.

C. Söderberg-Nauclér and J.Z. Haeggström contributed equally to this work.


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