Cox-2 inhibition abrogates Chlamydia pneumoniae-induced PGE2 and MMP-1 expression
Section snippets
Materials and methods
Culture of C. pneumoniae. The coronary artery isolate C. pneumoniae CV-6 was grown on immortalized laryngeal epithelial cell (HEp-2, ATCC CLL 23) monolayers as described previously [15]. Confluent monolayers were infected with C. pneumoniae and growth medium was replaced by an antibiotic-free medium (Eagle’s minimum essential medium; Sigma, Taufkirchen, Germany). HEp-2 cells cultured under identical conditions served as mock control.
Isolation of human blood monocytes. Blood monocytes (PBMC)
Infection of blood monocytes with C. pneumoniae
Chlamydia pneumoniae efficiently infected blood monocytes (>97%) from healthy volunteers. Chlamydial elementary bodies were rapidly ingested, and filled out the whole cytoplasm of infected mononuclear cells, showing the typical aberrant morphology of the persistent state after 48 h (Fig. 1B). Viability of C. pneumoniae infected PBMC, as shown with live/dead staining, proved that >95% of PBMC were still alive after 48 h (Fig. 1A).
Induction of the p38 and p44/42 MAPkinases in C. pneumoniae infected PBMC
Phosphorylation of the p38 and p44/42 MAPkinases in PBMC was
Discussion
The recruitment and accumulation of PBMC in the damaged vascular wall represent a central point towards plaque progression in atherosclerotic lesion formation [3]. PBMC, which are crucially involved in the innate immune response against infectious pathogens, have been described as persistently infected with C. pneumoniae in 5–25% of patients with coronary artery disease (CAD) [7], [8], [18]. We were thus interested to analyse whether chlamydial infection of PBMC, which appears refractory to
Acknowledgements
This study was supported by a grant from the Deutsche Forschungsgemeinschaft (SFB 367/ B11 and SPP1130, Ma2070/4-1). We thank T. Luedemann, A. Hellberg, and A. Gravenhorst (University of Luebeck) for technical assistance.
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