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肺炎衣原体感染加速载脂蛋白E缺乏小鼠的动脉粥样硬化进程。

Chlamydia pneumoniae infection accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

作者信息

Moazed T C, Campbell L A, Rosenfeld M E, Grayston J T, Kuo C C

机构信息

Immunobiology Department, Immunex Crporation, Seattle, WA 98101-2936, USA.

出版信息

J Infect Dis. 1999 Jul;180(1):238-41. doi: 10.1086/314855.

Abstract

Accumulating evidence supports an association between Chlamydia pneumoniae infection and atherosclerosis. To determine whether there is a causal relationship, the effects of chronic infection with C. pneumoniae on the development of atherosclerosis in apolipoprotein E (apoE)-deficient mice were evaluated. Eight-week-old male apoE-deficient mice were inoculated intranasally with C. pneumoniae three times, at 8, 9, and 10 weeks of age. The combined area of atherosclerotic lesions in the lesser curvature of the aortic arch was measured en face by computer-assisted morphometry. The lesion area was 2.4-fold greater (P=.05) at 16 weeks of age and 1.6-fold greater (P=.05) at 20 weeks of age in infected mice than in control mice. There were no differences in total plasma cholesterol levels between groups. This study demonstrates that C. pneumoniae infection accelerates the progression of atherosclerosis in the aortic arch of apoE-deficient mice.

摘要

越来越多的证据支持肺炎衣原体感染与动脉粥样硬化之间存在关联。为了确定是否存在因果关系,评估了肺炎衣原体慢性感染对载脂蛋白E(apoE)缺陷小鼠动脉粥样硬化发展的影响。8周龄的雄性apoE缺陷小鼠在8、9和10周龄时经鼻接种肺炎衣原体3次。通过计算机辅助形态测量法对主动脉弓小弯处动脉粥样硬化病变的总面积进行整体测量。在16周龄时,感染小鼠的病变面积比对照小鼠大2.4倍(P = 0.05),在20周龄时大1.6倍(P = 0.05)。各组之间的总血浆胆固醇水平没有差异。这项研究表明,肺炎衣原体感染会加速apoE缺陷小鼠主动脉弓处动脉粥样硬化的进展。

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