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Chlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.

Cell Metab.. 2018; 
Tumurkhuu Gantsetseg,Dagvadorj Jargalsaikhan,Porritt Rebecca A,Crother Timothy R,Shimada Kenichi,Tarling Elizabeth J,Erbay Ebru,Arditi Moshe,Chen Sh
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摘要

Pathogen burden accelerates atherosclerosis, but the mechanisms remain unresolved. Activation of the NLRP3 inflammasome is linked to atherogenesis. Here we investigated whether Chlamydia pneumoniae (C.pn) infection engages NLRP3 in promoting atherosclerosis. C.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr mice. C.pn-induced acceleration of atherosclerosis was significantly dependent on NLRP3 and caspase-1. We discovered that C.pn-induced extracellular IL-1β triggers a negative feedback loop to inhibit GPR109a and ABCA1 expression and cholesterol efflux, leading to accumulation of intracellular cholesterol and foam ce... More

关键词

ABCA1,C.?pneumoniae,Gpr109a,Nlrp3,aspartate,atherosclerosis,cholesterol efflux,foam cells,interleukin-1 beta,ni