Chylomicron Remnants Stimulate Release of Interleukin-1β by THP-1 Cells

Abstract

Recent findings suggest that the oxidative modification of low-density lipoproteins (LDL) and an increase in triglyceride-rich lipoprotein particles including chylomicron remnants contribute to the progression of atherosclerosis, as does the inflammatory response. We therefore examined whether and how these lipoproteins affected interleukin (IL)-1β release and mRNA expression for IL-1β and IL-18 in THP-1 cells, a human monocyte cell line. Chylomicron remnants increased IL-1β release into the conditioned medium by THP-1 in a dose- and time-dependent manner. At concentrations up to 1 μg/ml, chylomicron remnants increased IL-1β release by 4-fold compared with the control. Neither native LDL nor oxidized LDL (OxLDL) significantly increased IL-1β release. Chylomicron remnants increased IL-1β mRNA expression by 3 times. Native LDL or OxLDL did not increase IL-1β mRNA, while neither these lipoproteins nor chylomicron remnants increased IL-18 mRNA. Chylomicron remnants also increased the activities of caspase-1 and nuclear factor (NF)-κB significantly, while native LDL or OxLDL did not. In conclusion, chylomicron remnants stimulated IL-1β mRNA expression and IL-1β protein production probably via caspase-1 and NF-κB activation in THP-1 cells.