2010•Inter J Epidemiol Infect DisRequires access

Regulatory mechanism of lipoprotein on LPS-induced monocyte activation

Kuangyi Shu, Fang-Qu Li, Jin-hong Yang, Yang Ai-ping, Hongqun Tao, Hui Chen, Xiangyang Li

Open publisher page 0 citations

Abstract

Objective To investigate the affect mechanism of serum lipoproteins(HDL, LDL, VLDL) on LPS,and compare the regulation ability in LPS-activated of them, to provide theoretical basis for the application of lipoprotein in treatment of sepsis. Methods TNF-α secreted from PMA-differentiated THP-1 cell were detected to reflect the inhibitory action of lipoprotein on LPS indirectly. THP-1 cell were incubated with LPS for 4 houris, TNF-α levels were detected and then compared with the levels in which THP-1 cell incubated with lipoprotein-LPS mixture. Futhermore, the inhibitory action from lipoprotein to LPS was estimated. Results HDL, LDL and VLDL did not induce differentiated THP-1 cells to secrete TNF-α( P > 0.05). When lipoprotein was above 0.05 mg/mL and mixed with 10 ng/mL LPS,TNF-α decreased obviously. The inhibition action of 0. 1 mg/mL lipoprotein (HDL, LDL, VLDL) on LPS was low when LPS was 100 ng/mL, and the rates were (20.7± 11.1)%, (8.85+2.75)%, (4.3± 1.6)% respectively; the inhibitory effect was significantly increased when LPS was 10 ng/mL, and the rates were (69.3±3.7)%, (42.9±5.7)%,(42.7±4.5)% respectively. HDL had stronger inhibitory effect than LDL and VLDL(P < 0.05). ConclusionsLipoprotein in serum can inhibit LPS-activated macrophage cells to secrete cytolines, but the inhibition of lipoprotein is more obvious in high concentration of LPS than low concentration. HDL has a stronger inhibitory effect on LPS activation than LDL and VLDL. Key words: Lipopolysaccharicdes; Lipoproteins; Tumor necrosis factor-α

About this research paper

What this paper is about

Objective To investigate the affect mechanism of serum lipoproteins(HDL, LDL, VLDL) on LPS,and compare the regulation ability in LPS-activated of them, to provide theoretical basis for the application of lipoprotein in treatment of sepsis. Methods TNF-α secreted from PMA-differentiated THP-1 cell were detected to reflect the inhibitory action of lipoprotein on LPS indirectly. THP-1 cell were incubated with LPS for 4 houris, TNF-α levels were detected and then compared with the levels in which THP-1 cell incubated with lipoprotein-LPS mixture. Futhermore, the inhibitory action from lipoprotein to LPS was estimated. Results HDL, LDL and VLDL did not induce differentiated THP-1 cells to secrete TNF-α( P > 0.05). When lipoprotein was above 0.05 mg/mL and mixed with 10 ng/mL LPS,TNF-α decreased obviously. The inhibition action of 0. 1 mg/mL lipoprotein (HDL, LDL, VLDL) on LPS was low when LPS was 100 ng/mL, and the rates were (20.7± 11.1)%, (8.85+2.75)%, (4.3± 1.6)% respectively; the inhibitory effect was significantly increased when LPS was 10 ng/mL, and the rates were (69.3±3.7)%, (42.9±5.7)%,(42.7±4.5)% respectively. HDL had stronger inhibitory effect than LDL and VLDL(P < 0.05). ConclusionsLipoprotein in serum can inhibit LPS-activated macrophage cells to secrete cytolines, but the inhibition of lipoprotein is more obvious in high concentration of LPS than low concentration. HDL has a stronger inhibitory effect on LPS activation than LDL and VLDL. Key words: Lipopolysaccharicdes; Lipoproteins; Tumor necrosis factor-α

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To investigate the affect mechanism of serum lipoproteins(HDL, LDL, VLDL) on LPS,and compare the regulation ability in LPS-activated of them, to provide theoretical basis for the application of lipoprotein in treatment of sepsis. Methods TNF-α secreted from PMA-differentiated THP-1 cell were detected to reflect the inhibitory action of lipoprotein on LPS indirectly. THP-1 cell were incubated with LPS for 4 houris, TNF-α levels were detected and then compared with the levels in which THP-1 cell incubated with lipoprotein-LPS mixture. Futhermore, the inhibitory action from lipoprotein to LPS was estimated. Results HDL, LDL and VLDL did not induce differentiated THP-1 cells to secrete TNF-α( P > 0.05). When lipoprotein was above 0.05 mg/mL and mixed with 10 ng/mL LPS,TNF-α decreased obviously. The inhibition action of 0. 1 mg/mL lipoprotein (HDL, LDL, VLDL) on LPS was low when LPS was 100 ng/mL, and the rates were (20.7± 11.1)%, (8.85+2.75)%, (4.3± 1.6)% respectively; the inhibitory effect was significantly increased when LPS was 10 ng/mL, and the rates were (69.3±3.7)%, (42.9±5.7)%,(42.7±4.5)% respectively. HDL had stronger inhibitory effect than LDL and VLDL(P < 0.05). ConclusionsLipoprotein in serum can inhibit LPS-activated macrophage cells to secrete cytolines, but the inhibition of lipoprotein is more obvious in high concentration of LPS than low concentration. HDL has a stronger inhibitory effect on LPS activation than LDL and VLDL. Key words: Lipopolysaccharicdes; Lipoproteins; Tumor necrosis factor-α

Key concepts: Very low-density lipoprotein, Lipoprotein, Chemistry, Lipopolysaccharide, Endocrinology, Secretion, Internal medicine, Monocyte

Related papers

Back to paper searchBrowse research topicsOriginal source
Regulatory mechanism of lipoprotein on LPS-induced monocyte activation — Research Paper | ScholarLens