TY - GEN
T1 - Chronic infections and atherosclerosis
AU - Ayada, Kiyoshi
AU - Yokota, Kenji
AU - Kobayashi, Kazuko
AU - Shoenfeld, Yehuda
AU - Matsuura, Eiji
AU - Oguma, Keiji
PY - 2007/6
Y1 - 2007/6
N2 - Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti-heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe+/-ldlr+/- mice and that Hp-anti-heat-shock protein specific Th1-dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti-HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis.
AB - Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti-heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe+/-ldlr+/- mice and that Hp-anti-heat-shock protein specific Th1-dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti-HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis.
KW - Anti-heat shock protein (HSP60)
KW - Atherosclerosis
KW - Helicobacter pylori (H. pylori)
UR - http://www.scopus.com/inward/record.url?scp=34948853766&partnerID=8YFLogxK
U2 - 10.1196/annals.1422.062
DO - 10.1196/annals.1422.062
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C2 - 17894024
AN - SCOPUS:34948853766
SN - 157331708X
SN - 9781573317085
T3 - Annals of the New York Academy of Sciences
SP - 594
EP - 602
BT - Autoimmunity, Part D
PB - Blackwell Publishing Inc.
ER -