Abstract:
:In the presence of low density lipoprotein (LDL), Chlamydia pneumoniae induces macrophage-derived foam cell formation, a typical pathological feature of early atherosclerosis. However, its mechanism has not been fully understood. Peroxisome proliferator-activated receptors (PPARs) are key regulators of macrophage lipid metabolism. This study therefore investigated the role that PPAR alpha and PPAR gamma may play a role in C. pneumoniae-induced foam cell formation. Oil Red O staining and Lipid mass quantification showed that LDL-treated THP-1 macrophages infected with high doses of C. pneumoniae (5x10(5) and 1x10(6)IFU) resulted in the large accumulation of lipid droplets and markedly increased the ratio of intracellular cholesteryl ester (CE) to total cholesterol (TC) (>50%). The results of RT-PCR and Western blot indicated that C. pneumoniae infection dose-dependently suppressed the expression of PPAR alpha and PPAR gamma at mRNA and protein levels in LDL-treated THP-1 macrophages. PPAR alpha (fenofibrate) and PPAR gamma (rosiglitazone) agonists, inhibited the accumulation of intracellular CE by C. pneumoniae in a dose-dependent manner. Furthermore, C. pneumoniae-induced foam cell formation was significantly suppressed by higher doses of fenofibrate (20 and 50microM) and rosiglitazone (10 and 20microM). These results first reveal that C. pneumoniae induces foam cell formation via PPAR alpha and PPAR gamma-dependent pathway, which may contribute to its pro-atherogenic properties.
journal_name
Cell Biol Intjournal_title
Cell biology internationalauthors
Mei CL,He P,Cheng B,Liu W,Wang YF,Wan JJdoi
10.1016/j.cellbi.2008.12.002subject
Has Abstractpub_date
2009-03-01 00:00:00pages
301-8issue
3eissn
1065-6995issn
1095-8355pii
S1065-6995(08)00646-Xjournal_volume
33pub_type
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