The effect of cytokines produced by human adipose tissue on monocyte adhesion to the endothelium

Cell Adh Migr. 2019 Dec;13(1):293-302. doi: 10.1080/19336918.2019.1644856.

Abstract

Visceral adipose tissue (VAT) may play a critical role in atherosclerotic cardiovascular disease. The goal of this study was to determine the effect of human VAT-released pro‑inflammatory cytokines on monocyte adhesion to the endothelium. The cytokine effects on monocyte adhesion to the endothelial cells (ECs) were tested using adipose tissue-conditioned media (ATCM) prepared by culturing human VAT. The cytokines concentrations in ATCM, the cytokines expression and adhesion molecules in stimulated ECs were measured. The concentrations of IL-1β,TNF-α,MCP-1,IL-10,and RANTES measured in ATCM correlated positively with monocyte adhesiveness to ECs. Additionally, ATCM increased the adhesion molecules (ICAM-1, VCAM-1) gene expression. Selective inhibitors highlighted the importance of IL-1β and TNF-α in the process by a significant decrease in monocyte adhesion compared to ATCM preconditioning without inhibitors. Human VAT significantly increased monocyte adhesion to ECs. It was significantly influenced by IL-1β, TNF-α, MCP-1, IL-10, and RANTES, with IL-1β and TNF‑α having the strongest impact.

Keywords: Atherosclerosis; adipose tissue; cytokines; endothelium; inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Atherosclerosis / pathology
  • Cell Adhesion / physiology*
  • Cells, Cultured
  • Culture Media, Conditioned / pharmacology
  • Cytokines / metabolism*
  • Endothelial Cells / metabolism
  • Endothelium, Vascular / metabolism*
  • Humans
  • Intercellular Adhesion Molecule-1 / metabolism
  • Intra-Abdominal Fat / metabolism*
  • Middle Aged
  • Monocytes / metabolism*
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Culture Media, Conditioned
  • Cytokines
  • ICAM1 protein, human
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1

Grants and funding

The project was supported by the Charles University Grant Agency, project GA UK No. 592216, and Ministry of Health, Czech Republic for the development of research organization 00023001 (Institute for Clinical and Experimental Medicine, Prague, Czech Republic) for institutional support. Grantová Agentura, Univerzita Karlova [592216]; Ministerstvo Zdravotnictví Ceské Republiky [00023001].