Fusobacterium nucleatum GroEL signaling via Toll-like receptor 4 in human microvascular endothelial cells
0
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
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-κB 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 TLR4knockdown. 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-κB pathways.
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-κB 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 TLR4knockdown. 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-κB pathways.
참고문헌 (16)
- 백은정, "Inhibitory Effect of SPA0355, a Thiourea Analogue, on Inflammation and Alveolar Bone Loss in Rats with Ligature-Induced Periodontitis", International Journal of Oral Biology, 37(2), pp.63~68 (2012), 대한구강생물학회[DOI]
- Hwa Jung CHOI, "Protective Effect of HP08-0106 on Ligature-induced Periodontitis in Rats", International Journal of Oral Biology, 36(4), pp.187~194 (2011), 대한구강생물학회
- Ayada K, "Chronic infections and atherosclerosis", Clin Rev Allergy Immunol, 37, pp.44~48 (2009)
- Wick G, "Atherosclerosis as an autoimmune disease: an update", Trends Immunol, 22, pp.665~669 (2001)
- Tabeta K, "Elevated humoral immune response to heat shock protein 60 (hsp60) family in periodontitis patients", Clin Exp Immunol, 120, pp.285~293 (2000)
- Kolenbrander PE, "Oral multispecies biofilm development and the key role of cell-cell distance", Nat Rev Microbiol, 8, pp.471~480 (2010)
- Ford PJ, "Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study", Oral Microbiol Immunol, 21, pp.206~211 (2006)
- 전혜경, "Fusobacterium nucleatum GroEL induces risk factors of atherosclerosis in human microvascular endothelial cells and ApoE -", - mice, 201204, pp.27(2), 109~123[DOI]
- Wang W, "TLR4 activation induces nontolerant inflammatory response in endothelial cells", Inflammation, 34, pp.509~518 (2011)
- Kol A, "Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages", J Clin Invest, 103, pp.571~577 (1999)
- Graham GM, "Proinflammatory cytokine production by human keratinocytes stimulated with Propionibacterium acnes and P. acnes GroEL", Br J Dermatol, 150, pp.421~428 (2004)
- Baranova IN, "Class B scavenger receptor types I and II and CD36 mediatebacterial recognition and proinflammatory signaling induced by Escherichia coli, lipopolysaccharide, and cytosolic chaperonin 60", J Immunol, 188, pp.1371~1380 (2012)
- Vabulas RM, "Endocytosed HSP60s use Toll-like receptor 2 (TLR2) and TLR4 to activate the toll", interleukin-1 receptor signaling pathway in innate immune cells, 2001, pp.276, 31332~31339
- Argueta JG, "Induction of Porphyromonas gingivalis GroEL signaling via binding to Toll-like receptors 2 and 4", Oral Microbiol Immunol, 21, pp.245~251 (2006)
- Faure E, "Bacterial lipopolysaccharide activates NF-κB through toll-like receptor 4 (TLR-4) in cultured human dermal endothelial cells. Differential expression of TLR-4 and TLR-2 in endothelial cells", J Biol Chem, 275, pp.11058~11063 (2000)
- Han SH, "Pneumococcal lipoteichoic acid (LTA) is not as potent as staphylococcal LTA in stimulating Toll-like receptor 2", Infect Immun, 71, pp.5541~5548 (2003)