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Genital Chlamydia infection in hyperlipidemic mouse models exacerbates atherosclerosis.

Abstract：

BACKGROUND AND AIMS:Atherosclerosis is a chronic inflammatory disease, and recent studies have shown that infection at remote sites can contribute to the progression of atherosclerosis in hyperlipidemic mouse models. In this report, we tested the hypothesis that genital Chlamydia infection could accelerate the onset and progression of atherosclerosis. METHODS:Apolipoprotein E (Apoe-/-) and LDL receptor knockout (Ldlr-/-) mice on a high-fat diet were infected intra-vaginally with Chlamydia muridarum. Atherosclerotic lesions on the aortic sinuses and in the descending aorta were assessed at 8-weeks post-infection. Systemic, macrophage, and vascular site inflammatory responses were assessed and quantified. RESULTS:Compared to the uninfected groups, infected Apoe-/- and Ldlr-/- mice developed significantly more atherosclerotic lesions in the aortic sinus and in the descending aorta. Increased lesions were associated with higher circulating levels of serum amyloid A-1, IL-1β, TNF-α, and increased VCAM-1 expression in the aortic sinus, suggesting an association with inflammatory responses observed during C. muridarum infection. Genital infection courses were similar in Apoe-/-, Ldlr-/-, and wild type mice. Further, Apoe-/- mice developed severe uterine pathology with increased dilatations. Apoe-deficiency also augmented cytokine/chemokine response in C. muridarum infected macrophages, suggesting that the difference in macrophage response could have contributed to the genital pathology in Apoe-/- mice. CONCLUSIONS:Overall, these studies demonstrate that genital Chlamydia infection exacerbates atherosclerotic lesions in hyperlipidemic mouse and suggest a novel role for Apoe in full recovery of uterine anatomy after chlamydial infection.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Nagarajan UM,Sikes JD,Burris RL,Jha R,Popovic B,Fraungruber P,Hennings L,Haggerty CL,Nagarajan S

doi

10.1016/j.atherosclerosis.2019.09.021

subject

Has Abstract

pub_date

2019-11-01 00:00:00

pages

103-110

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(19)31508-4

journal_volume

290

pub_type

杂志文章

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