Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation

Atherosclerosis. 2016 May:248:170-8. doi: 10.1016/j.atherosclerosis.2016.03.012. Epub 2016 Mar 10.

Abstract

Background: In atherosclerotic lesions, cholesterol-laden macrophage foam cells are formed and exposed to M1- and M2-polarizing factors. However, the effects of the polarizing factors on the proinflammatory and the anti-inflammatory potential of foam cells are not known.

Objective: To investigate the effects of M1- and M2-polarizing factors on the expression of pro- and anti-inflammatory genes in cultured human macrophage foam cells.

Methods and results: Human monocytes were differentiated into macrophages in the presence of M-CSF, and then converted into cholesterol-loaded foam cells by incubation with acetylated LDL. The generated macrophages and foam cells were polarized into the M1 phenotype by classical activation with LPS and IFN-γ, or into the M2 phenotype by alternative activation with IL-4. When subjected to the M1-polarizing factors, the macrophages responded by typical upregulation of several key proinflammatory genes (TNFA, IL1B, CXCL8, CCL19, and COX2), while the anti-inflammatory genes (MRC1, CCL17, and IL10) displayed variable responses. The foam cells, again, showed a weaker response to the M1-polarizing factors, as indicated by reduced upregulation of the proinflammatory genes, reduced secretion of TNF-α, and a trend towards lower NF-κB activity. When subjected to alternative M2 polarization, both macrophages and foam cells responded by a typical upregulation of the anti-inflammatory genes, which was of equal magnitude in both cell types.

Conclusions: Conversion of cultured human macrophages into foam cells suppresses their proinflammatory responses to M1-polarizing factors. Thus, in M1-polarizing microenvironments of atherosclerotic lesions, foam cell formation may locally weaken the macrophage-dependent inflammatory component of atherogenesis.

Keywords: Atherosclerosis; Cytokines; Foam cells; Inflammation; Macrophages; Polarization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents / chemistry
  • Atherosclerosis / metabolism
  • Cholesterol / chemistry
  • Cholesterol / metabolism
  • Culture Media, Serum-Free
  • Foam Cells / cytology*
  • Gene Expression Regulation
  • Humans
  • Inflammation / metabolism
  • Interferon-gamma / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-4 / metabolism
  • Lipopolysaccharides / chemistry
  • Macrophage Colony-Stimulating Factor / metabolism*
  • Macrophages / cytology*
  • Macrophages / metabolism
  • NF-kappa B / metabolism
  • Phenotype
  • Up-Regulation

Substances

  • Anti-Inflammatory Agents
  • Culture Media, Serum-Free
  • Interleukin-1beta
  • Lipopolysaccharides
  • NF-kappa B
  • Interleukin-4
  • Macrophage Colony-Stimulating Factor
  • Interferon-gamma
  • Cholesterol