Eikenella corrodens lipopolysaccharide stimulates the pro-atherosclerotic response in human coronary artery endothelial cells and monocyte adhesion

Autores organización

• Diego Fernando Gualtero Escobar

  Autor

• 

  Gloria Ines Lafaurie Villamil

  Autor

Autores

• Viafara-Garcia S.M.
• Avila-Ceballos D.

Unidades de investigación

• Unidad de Investigación Básica Oral UIBO

  

  Investigador

  Gloria Ines Lafaurie Villamil

Resumen

Eikenella corrodens is a gram-negative bacterium, and although primarily associated with periodontal infections or infective endocarditis, it has been identified in coronary atheromatous plaques. The effect of its lipopolysaccharide (LPS) on human coronary artery endothelial cells (HCAECs) is unknown. Our aim was to examine the mechanism underlying the inflammatory response in HCAECs stimulated with E. corrodens-LPS and to evaluate monocyte adhesion. Endothelial responses were determined by measuring the levels of chemokines and cytokines using flow cytometry. The surface expression of intercellular adhesion molecule 1 (ICAM-1) was determined using a cell-based ELISA, and the adhesion of THP-1 monocytes to HCAECs was also monitored. The involvement of toll-like receptors (TLRs) 2 and 4 was examined using TLR-neutralizing antibodies, and activation of extracellular signal-regulated kinase (ERK)1/2 and nuclear factor-kappa B (NF-?B) p65 were measured by western blotting and ELISA, respectively. Eikenella corrodens-LPS increased secretion of interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and granulocyte–macrophage colony-stimulating factor (GM-CSF), and expression of ICAM-1 on the surface of HCAECs, consistent with the increased adhesion of THP-1 cells. Moreover, E. corrodens-LPS interacted with TLR4, a key receptor able to maintain the levels of IL-8, MCP-1, and GM-CSF in HCAECs. Phosphorylation of ERK1/2 and activation of NF-?B p65 were also increased. The results indicate that E. corrodens-LPS activates HCAECs through TLR4, ERK, and NF-?B p65, triggering a pro-atherosclerotic endothelial response and enhancing monocyte adhesion. © 2018 Eur J Oral Sci

Keywords

• Antibodies, Neutralizing; Cell Adhesion; Cell Survival; Cells, Cultured; Chemokine CCL2; Chemokines; Coronary Artery Disease; Coronary Vessels; Cytokines; Eikenella corrodens; Endothelial Cells; Granulocyte-Macrophage Colony-Stimulating Factor; Humans; Intercellular Adhesion Molecule-1; Interleukin-8; Lipopolysaccharides; Mitogen-Activated Protein Kinases; Monocytes; NF-kappa B; Phosphorylation; THP-1 Cells; Toll-Like Receptor 2; Toll-Like Receptor 4; chemokine; cytokine; granulocyte macrophage colony stimulating factor; IL8 protein, human; immunoglobulin enhancer binding protein; intercellular adhesion molecule 1; interleukin 8; lipopolysaccharide; mitogen activated protein kinase; monocyte chemotactic protein 1; neutralizing antibody; TLR2 protein, human; TLR4 protein, human; toll like receptor 2; toll like receptor 4; cell adhesion; cell culture; cell survival; chemically induced; coronary artery disease; coronary blood vessel; drug effect; Eikenella corrodens; endothelium cell; hum