C. pneumoniae infection stimulates LDL oxidization and uptake and foam cell formation in macrophages (12,13). Furthermore, a previous study by our group indicated that C. pneumoniae induced macrophage‐derived foam cell formation through upregulation of the expression of scavenger receptor
نویسندگان
چکیده
Atherosclerosis is well established as a chronic inflammatory disorder, and Chlamydia pneumoniae is considered to be a risk factor for atherosclerotic development. Endothelial dysfunction, caused by oxidized low‐density lipoprotein (ox‐LDL) is an early atherosclerotic marker. However, the effect of C. pneumoniae on lipid metabolism in vascular endothelial cells is yet to be elucidated. The aim of the present study was to investigate the effects of C. pneumoniae on lipid metabolism in human umbilical vein endothelial cells (HUVECs). In the present study, LDL oxidation was found to be significantly induced in the supernatant, but not the cell lysates, of C. pneumoniae-infected HUVECs. Furthermore, C. pneumoniae infection was observed to increase the levels of total cholesterol and cholesteryl esters in LDL‐treated HUVECs. In addition, C. pneumoniae was found to upregulate the expression of scavenger receptor A, cluster of differentiation 36 and acyl‐coenzyme A: cholesterol acyltransferase 1 mRNA and protein. C. pneumoniae was also observed to downregulate the mRNA and protein expression of ATP binding cassette transporter (ABC) A1 and ABCGl in LDL‐treated HUVECs. These results show that C. pneumoniae disrupts lipid metabolism in HUVECs.
منابع مشابه
Inhibitory effect of Cinnamon on prevention of foam cell formation in platelet and monocytes co-culture
Introduction: Atherosclerosis is one of the leading causes of cardiovascular disease. Following endothelial damage and platelet aggregation in that area and the recruitment of monocytes and their conversion to macrophages, LDL gradually accumulates under the endothelial artery wall and gradually oxidized and convert to oxi-LDL. By swallowing it, the macrophages turn into foam cell and then athe...
متن کاملA Chlamydia pneumoniae component that induces macrophage foam cell formation is chlamydial lipopolysaccharide.
Chlamydia pneumoniae infection is associated with atherosclerotic heart and vessel disease, but a causal relationship between this pathogen and the disease process has not been established. Recently, it was reported that C. pneumoniae induces human macrophage foam cell formation, a key event in early atheroma development, suggesting a role for the organism in atherogenesis. This study further e...
متن کاملFoam cell formation inhibits growth of Chlamydia pneumoniae but does not attenuate Chlamydia pneumoniae-induced secretion of proinflammatory cytokines.
BACKGROUND It has not yet been determined whether lipid-loaded macrophages (foam cells), a major cellular component of atherosclerotic lesions, have the capacity to support growth of Chlamydia pneumoniae and be activated to secrete proinflammatory cytokines in response to C pneumoniae infection. METHODS AND RESULTS Lipid loading of RAW 264.7 cells and mouse peritoneal macrophages with either ...
متن کاملLow-density lipoprotein from apolipoprotein E-deficient mice induces macrophage lipid accumulation in a CD36 and scavenger receptor class A-dependent manner.
OBJECTIVE To investigate the potential of circulating low-density lipoprotein (LDL), isolated from apolipoprotein E (apoE)-deficient mice (E-/-LDL) and from LDL receptor-deficient mice (Lr-/-LDL), to induce foam cell formation. METHODS AND RESULTS Binding studies using COS-7 cells overexpressing CD36, J774 cells, and mouse peritoneal macrophages (MPMs) unexpectedly showed for the first time t...
متن کاملInhibition of protein kinase Cbeta prevents foam cell formation by reducing scavenger receptor A expression in human macrophages.
BACKGROUND Low-density lipoprotein (LDL) uptake by monocyte-derived macrophages is a crucial step in foam cell formation and early atherosclerotic lesion. Increasing evidence supports the theory that activation of protein kinase Cbeta (PKCbeta) is involved in many mechanisms promoting atherosclerosis. Thus, we investigated whether inhibition of PKCbeta prevents foam cell formation. METHODS AN...
متن کامل