Research Topics
| Chie HayashiSummaryAffiliation: Boston University Country: USA Publications
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Detail Information
Publications
Porphyromonas gingivalis accelerates inflammatory atherosclerosis in the innominate artery of ApoE deficient miceChie Hayashi
Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, 650 Albany Street, Boston, MA 02118, United States
Atherosclerosis 215:52-9. 2011..gingivalis infection accelerates inflammation and atherosclerosis in the innominate artery of mice, an artery which has been reported to exhibit many features of human atherosclerotic disease, including plaque rupture...
Protective role for TLR4 signaling in atherosclerosis progression as revealed by infection with a common oral pathogenChie Hayashi
Section of Infectious Diseases, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
J Immunol 189:3681-8. 2012..We demonstrate an atheroprotective role for TLR4 in response to infection with the oral pathogen P. gingivalis. Our results point to a role for pathogen-specific TLR signaling in chronic inflammation and atherosclerosis...
Pathogen-mediated inflammatory atherosclerosis is mediated in part via Toll-like receptor 2-induced inflammatory responsesChie Hayashi
Department of Medicine, Sections of Infectious Diseases, Boston University School of Medicine, Boston, MA 02118, USA
J Innate Immun 2:334-43. 2010..gingivalis-infected TLR2-deficient (TLR2(-/-)) mice. These studies provide a mechanistic link between an innate immune receptor and pathogen-accelerated atherosclerosis by a clinically and biologically relevant bacterial pathogen...
Stimulation of Toll-like receptor 2 in human platelets induces a thromboinflammatory response through activation of phosphoinositide 3-kinasePrice Blair
Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston, MA 02118 2526, USA
Circ Res 104:346-54. 2009..This work substantiates the role of platelets in the immune and inflammatory response and suggests a mechanism by which bacteria could directly activate platelets...
