Fusobacterium nucleatum GroEL signaling via Toll-like receptor 4 in human microvascular endothelial cells
International Journal of Oral Biology
;
: 130-136, 2012.
Article
in English
| WPRIM
| ID: wpr-222608
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Periodontitis
/
Thromboplastin
/
Risk Factors
/
Interleukin-8
/
NF-kappa B
/
Fusobacterium nucleatum
/
Intercellular Adhesion Molecule-1
/
Vascular Cell Adhesion Molecule-1
/
Chemokine CCL2
/
E-Selectin
Type of study:
Etiology study
/
Prognostic study
/
Risk factors
Limits:
Animals
/
Humans
Language:
English
Journal:
International Journal of Oral Biology
Year:
2012
Type:
Article
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