Fusobacterium nucleatum GroEL signaling via Toll-like receptor 4 in human microvascular endothelial cells.
- Author:
Hae Ri LEE
1
;
Bong Kyu CHOI
Author Information
1. Korea Centers for Disease Centers for Disease Control and Prevention, Cheongwon-gun, Chungbuk, Korea.
- Publication Type:Original Article
- Keywords:
Fusobacterium nucleatum;
GroEL;
Periodontitis;
Signaling
- MeSH:
Animals;
Atherosclerosis;
Chemokine CCL2;
E-Selectin;
Endothelial Cells;
Fusobacterium;
Fusobacterium nucleatum;
Heat-Shock Proteins;
Humans;
Intercellular Adhesion Molecule-1;
Interleukin-8;
Mice;
NF-kappa B;
Periodontitis;
Risk Factors;
Thromboplastin;
Toll-Like Receptor 4;
Toll-Like Receptors;
Vascular Cell Adhesion Molecule-1
- From:International Journal of Oral Biology
2012;37(3):130-136
- CountryRepublic of Korea
- Language:English
-
Abstract:
The GroEL heat-shock protein from Fusobacterium nucleatum, a periodontopathogen, activates risk factors for atherosclerosis in human microvascular endothelial cells (HMEC-1) and ApoE-/- mice. In this study, we analyzed the signaling pathways by which F. nucleatum GroEL induces the proinflammatory factors in HMEC-1 cells known to be risk factors associated with the development of atherosclerosis and identified the cellular receptor used by GroEL. The MAPK and NF-kappaB signaling pathways were found to be activated by GroEL to induce the expression of interleukin-8 (IL-8), monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and tissue factor (TF). These effects were inhibited by a TLR4 knockdown. Our results thus indicate that TLR4 is a key receptor that mediates the interaction of F. nucleatum GroEL with HMEC-1 cells and subsequently induces an inflammatory response via the MAPK and NF-kappaB pathways.
