TY - JOUR
T1 - Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis
AU - Ayada, K.
AU - Yokota, K.
AU - Hirai, K.
AU - Fujimoto, K.
AU - Kobayashi, K.
AU - Ogawa, H.
AU - Hatanaka, K.
AU - Hirohata, S.
AU - Yoshino, T.
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
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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 -