Induction of macrophage foam cell formation by Chlamydia pneumoniae
Induction of macrophage foam cell formation by Chlamydia pneumoniae
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DOI：
10.1086/514241
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发表时间：
1998-03-01
影响因子：
6.4
通讯作者：
Byrne, GI
中科院分区：
文献类型：
--
作者：
Kalayoglu, MV;Byrne, GI
泡沫细胞的形成是早期动脉粥样硬化的标志。发现细胞内细菌肺炎衣原体诱导人单核细胞源性巨噬细胞形成泡沫细胞。巨噬细胞暴露于肺炎梭菌后，低密度脂蛋白（LDL）引起泡沫细胞数量的显著增加和胆固醇酯的积累。泡沫细胞的形成不受抗氧化剂丁基羟基甲苯和岩藻聚糖的抑制，这表明脂质积累与清道夫受体无关。相反，肝素的加入可以阻断LDL与LDL受体的结合，从而抑制肺炎假体诱导的泡沫细胞形成，这表明病原体通过失调天然LDL摄取或代谢（或两者兼而有之）诱导脂质积累。这些数据表明，感染因子可以诱导巨噬细胞泡沫细胞形成，并暗示肺炎原体是动脉粥样硬化的一个致病因素。
Foam cell formation is the hallmark of early atherosclerosis. It was found that the intracellular bacterium Chlamydia pneumoniae induces foam cell formation by human monocyte-derived macrophages. Exposure of macrophages to C. pneumoniae followed by low-density lipoprotein (LDL) caused a marked increase in the number of foam cells and accumulation of cholesteryl esters. Foam cell formation was not inhibited by the antioxidant butylated hydroxytoluene nor fucoidan, suggesting that lipid accumulation did not involve scavenger receptors. In contrast, addition of heparin, which blocks binding of LDL to the LDL receptor, inhibited C. pneumoniae-induced foam cell formation, suggesting that the pathogen induced lipid accumulation by dysregulating native LDL uptake or metabolism (or both). These data demonstrate that an infectious agent can induce macrophage foam cell formation and implicate C. pneumoniae as a causative factor in atherosclerosis.