Endothelial Chlamydia pneumoniae infection promotes oxidation of LDL

Ralf Dittrich*, Charalampos Dragonas, Andreas Mueller, Theodoros Maltaris, Jan Rupp, Matthias W. Beckmann, Matthias Maass

*Corresponding author for this work
20 Citations (Scopus)


The bacterium Chlamydia pneumoniae chronically infects atheromatous lesions and is linked to atherosclerosis by modifying inflammation, proliferation, and the lipid metabolism of blood monocytes. As continuous LDL modification in the vascular intima is crucial for atherogenesis we investigated the impact of endothelial infection on LDL oxidation. HUVEC were infected with a vascular C. pneumoniae strain. Supernatants of infected cells but not cell lysates increased lipid peroxidation products (6.44 vs 6.14nmol/ml, p<0.05) as determined by thiobarbituric acid reacting substances assay. Moreover, supernatants rendered human LDL more susceptible to oxidation as shown in a copper-ion catalysed LDL oxidation assay by a 16% reduction of LDL resistance against pro-oxidative stimuli (p<0.05). Chlamydial infection of vascular endothelial cells releases acellular components that convert LDL to its proatherogenic form and reduce its resistance against oxidation. Foci of chronic endothelial chlamydial infection may thus continuously contribute to the dysregulated lipid metabolism that promotes atherogenesis.

Original languageEnglish
JournalBiochemical and Biophysical Research Communications
Issue number2
Pages (from-to)501-505
Number of pages5
Publication statusPublished - 25.06.2004

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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