Chronic infections and atherosclerosis

Kiyoshi Ayada, Kenji Yokota, Kazuko Kobayashi, Yehuda Shoenfeld, Eiji Matsuura*, Keiji Oguma

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

39 Scopus citations

Abstract

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.

Original languageEnglish
Title of host publicationAutoimmunity, Part D
Subtitle of host publicationAutoimmune Disease, Annus Mirabilis
PublisherBlackwell Publishing Inc.
Pages594-602
Number of pages9
ISBN (Print)157331708X, 9781573317085
DOIs
StatePublished - Jun 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1108
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Anti-heat shock protein (HSP60)
  • Atherosclerosis
  • Helicobacter pylori (H. pylori)

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