Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis

K. Ayada, K. Yokota, K. Hirai, K. Fujimoto, K. Kobayashi, H. Ogawa, K. Hatanaka, S. Hirohata, T. Yoshino, Y. Shoenfeld, Eiji Matsuura*, K. Oguma

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Helicobacter pylori (H. pylori) is a predominant pathogen that causes not only gastroduodenal diseases but also extra-alimentary tract diseases. In this study, we demonstrated that H. pylori infection promoted atherogenesis in heterozygous apoe+/- ldlr+/- mice. The male mice were fed with high fat diet from the age of 6 weeks. At the age of 16 weeks, development of atherosclerotic lesions was observed in the H. pylori-infected mice, and it seemed to be associated with an elevation of Th1-immune response against H. pylori origin-heat shock protein 60 (Hp-HSP60) and an increment of transendothelial migration of T cells. Subcutaneous immunisation with Hp-HSP60 or H. pylori eradication with antibiotics significantly reduced the progression of atherosclerosis, accompanied by a decline of Th1 differentiation and reduction of their chemotaxis beyond the endothelium. Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis.

Original languageEnglish
Pages (from-to)1154-1168
Number of pages15
Issue number13
StatePublished - 2009


  • Atherosclerosis
  • Autoimmunity
  • Heat shock protein 60 (HSP60)
  • Helicobacter pylori (H. pylori
  • Hp)
  • Transendothelial migration


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