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Excess TNF-α in the blood activates monocytes with the potential to directly form cholesteryl ester-laden cells

Ming Zhu1, Lei Lei1, Zhenhua Zhu2

  • 1Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Acta Biochimica Et Biophysica Sinica
|September 17, 2015
PubMed

Insights

Excess tumor necrosis factor-alpha (TNF-α) in coronary heart disease (CHD) patients activates blood monocytes. This activation directly leads to cholesteryl ester-laden cells, a key factor in atherosclerosis development.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Atherosclerosis Research

Background:

  • Atherosclerosis, a primary cause of coronary heart disease (CHD), involves tumor necrosis factor-alpha (TNF-α) and monocytic cells.
  • Elevated levels of pro-inflammatory cytokines, including TNF-α, are observed in CHD patients compared to healthy individuals.

Purpose of the Study:

  • To investigate the impact of excess TNF-α on blood monocytes in the context of coronary heart disease (CHD).
  • To determine the correlation between plasma TNF-α levels and the potential of monocytes to form cholesteryl ester (CE)-laden cells.

Main Methods:

  • In vitro incubation of blood monocytes from CHD patients and healthy volunteers with oxidized low-density lipoprotein (oxLDL).
  • Measurement of plasma cytokine levels (TNF-α, IL-6, CRP) and correlation analysis with monocyte function.
  • Experiments using human blood monocytes and THP-1 cells to demonstrate TNF-α's activating effect, blocked by anti-TNF-α antibodies.
  • Assessment of TNF-α's influence on monocyte adhesion and oxLDL uptake via expression of adhesion molecules and scavenger receptors.
  • In vivo and in vitro studies using a mouse model to confirm findings.

Main Results:

  • Monocytes from CHD patients directly formed CE-laden cells when incubated with oxLDL in vitro.
  • Plasma TNF-α levels, but not IL-6 or CRP, positively correlated with the potential of monocytes to form CE-laden cells.
  • TNF-α significantly enhanced monocyte adhesion and oxLDL uptake by upregulating adhesion molecules and scavenger receptors.
  • The pro-atherogenic effect of TNF-α on monocytes was confirmed in a mouse model.

Conclusions:

  • Excess TNF-α in the blood is a primary trigger for the development of atherosclerosis and coronary heart disease (CHD).
  • TNF-α directly activates monocytes, promoting their transformation into CE-laden cells, thereby contributing to atherosclerotic plaque formation.

Keywords:
CE-laden cellTNF-αcholesteryl ester (CE)coronary heart disease (CHD)monocyteoxLDL

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