Chlamydia pneumoniae infection enhances lectin-like oxidized low-density lipoprotein receptor (LOX-1) expression on human endothelial cells.
Many studies indicate that Chlamydia pneumoniae infection is a crucial risk factor in atherogenesis. The most relevant cell type for the pathogenesis is the macrophage, which possesses classical scavenger receptors that uptake oxidized low-density lipoprotein (LDL). Here, a direct involvement of vascular endothelial cells in atherogenesis was examined employing in vitro infection of human umbilical vein endothelial cells (HUVEC) with C. pneumoniae. Chlamydia pneumoniae infection greatly enhanced the uptake of oxidized LDL, but not of acetylated LDL, by HUVEC. Among the scavenger receptors analyzed, LOX-1 transcription, which prefers oxidized LDL to acetylated LDL, was significantly amplified.
Yoshida
Tomoaki
T
Department of Microbiology and Immunology, Aichi Medical University, School of Medicine, Nagakute, Aichi, Japan. tomo@aichi-med-u.ac.jp
Koide
Naoki
N
Mori
Isamu
I
Ito
Hiroyasu
H
Yokochi
Takashi
T
D050197:Atherosclerosis / Q000209:etiology; D002478:Cells, Cultured; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D042783:Endothelial Cells / Q000378:metabolism*; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D051127:Scavenger Receptors, Class E / Q000235:genetics*
D008077:Lipoproteins, LDL; C495137:OLR1 protein, human; D051127:Scavenger Receptors, Class E; C032629:acetyl-LDL; C099252:oxidized low density lipoprotein