Helicobacter pylori infection enhances atherosclerosis in high-cholesterol diet fed C57BL/6 mice.
- Author:
Xing-hai CHEN
1
;
Jiang-bin WANG
;
Yu-shan WANG
;
Zhong-min LIU
;
Yan LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Atherosclerosis; microbiology; pathology; Bacterial Proteins; genetics; Bacterial Toxins; genetics; Cholesterol; blood; Cholesterol, Dietary; adverse effects; DNA, Bacterial; analysis; Female; Helicobacter Infections; pathology; Helicobacter pylori; genetics; Mice; Mice, Inbred C57BL; Triglycerides; blood; Urease; genetics
- From: Chinese Journal of Cardiology 2010;38(3):259-263
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the impacts of Helicobacter pylori (H. pylori) infection on atherosclerosis and plasma lipid levels in high-cholesterol diet fed C57BL/6 mice.
METHODFemale C57BL/6 mice were randomly divided into 4 groups (n = 12 each): fed with normal chow diet (A), infected with H. pylori (B), fed with high-cholesterol diet (C) and infected with H. pylori and fed with high-cholesterol diet (D). After 52 weeks, plasma levels of lipids were measured and aortic atherosclerosis was observed. The ureA, ureC, cagA and vacA DNA were also detected by PCR in the aortic arteries.
RESULT(1) Prevalence of atherosclerosis was similar between group C and D (91.6% vs. 100%, P > 0.05) while there was no atherosclerosis in group A and B. H. pylori infected mice showed more obvious inflammation in gastric mucosa than mice without H. pylori infection. (2) The plasma levels of triglyceride, total cholesterol and LDL were higher and HDL was lower in group B, C and D than those in group A and in group D than in group C (all P < 0.05). (3) Roberts & Thompson scores and number of foam cells in plaques were significantly higher in group D compared with those in group C (all P < 0.05). (4) ureC DNA was detected in 5 out of 12 aortic arteries of mice in group D but not in group A, B and C.
CONCLUSIONOur results suggested that H. pylori infection might enhance the atherosclerotic lesion formation in this mouse model.