Abstract
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 language | English |
|---|---|
| Pages (from-to) | 1154-1168 |
| Number of pages | 15 |
| Journal | Lupus |
| Volume | 18 |
| Issue number | 13 |
| DOIs | |
| Publication status | Published - 2009 |
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Keywords
- Atherosclerosis
- Autoimmunity
- Heat shock protein 60 (HSP60)
- Helicobacter pylori (H. pylori
- Hp)
- Transendothelial migration
ASJC Scopus subject areas
- Rheumatology
Cite this
Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis. / Ayada, K.; Yokota, Kenji; Hirai, K.; Fujimoto, K.; Kobayashi, Kazuko; Ogawa, Hiroko; Hatanaka, K.; Hirohata, Satoshi; Yoshino, Tadashi; Shoenfeld, Y.; Matsuura, Eiji; Oguma, K.
In: Lupus, Vol. 18, No. 13, 2009, p. 1154-1168.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis
AU - Ayada, K.
AU - Yokota, Kenji
AU - Hirai, K.
AU - Fujimoto, K.
AU - Kobayashi, Kazuko
AU - Ogawa, Hiroko
AU - Hatanaka, K.
AU - Hirohata, Satoshi
AU - Yoshino, Tadashi
AU - Shoenfeld, Y.
AU - Matsuura, Eiji
AU - Oguma, K.
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
KW - Atherosclerosis
KW - Autoimmunity
KW - Heat shock protein 60 (HSP60)
KW - Helicobacter pylori (H. pylori
KW - Hp)
KW - Transendothelial migration
UR - http://www.scopus.com/inward/record.url?scp=71049183037&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=71049183037&partnerID=8YFLogxK
U2 - 10.1177/0961203309106600
DO - 10.1177/0961203309106600
M3 - Article
C2 - 19880562
AN - SCOPUS:71049183037
VL - 18
SP - 1154
EP - 1168
JO - Lupus
JF - Lupus
SN - 0961-2033
IS - 13
ER -