Chylomicron remnants stimulate release of interleukin-1beta 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)-1beta release and mRNA expression for IL-1beta and IL-18 in THP-1 cells, a human monocyte cell line. Chylomicron remnants increased IL-1beta release into the conditioned medium by THP-1 in a dose- and time-dependent manner. At concentrations up to 1 microg/ml, chylomicron remnants increased IL-1beta release by 4-fold compared with the control. Neither native LDL nor oxidized LDL (OxLDL) significantly increased IL-1beta release. Chylomicron remnants increased IL-1beta mRNA expression by 3 times. Native LDL or OxLDL did not increase IL-1beta 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)-kappaB significantly, while native LDL or OxLDL did not. In conclusion, chylomicron remnants stimulated IL-1beta mRNA expression and IL-1beta protein production probably via caspase-1 and NF-kappaB activation in THP-1 cells.

journal_name

J Atheroscler Thromb

authors

Okumura T,Fujioka Y,Morimoto S,Masai M,Sakoda T,Tsujino T,Kashiwamura S,Okamura H,Ohyanagi M

doi

10.5551/jat.13.38

subject

Has Abstract

pub_date

2006-02-01 00:00:00

pages

38-45

issue

1

eissn

1340-3478

issn

1880-3873

pii

JST.JSTAGE/jat/13.38

journal_volume

13

pub_type

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