| Summary: | Thesis (M.A.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. === Atheroslcerosis is a progressive inflammatory disease of the human artery marked by accumulation of fatty, cellular, and fibrous material within the vessel wall. It is one of the main contributors to cardiovascular disease and is the main cause of death in the United States. The accumulation of material is a consequence of an innate immune reaction at the site of vessel wall injury and results in the chronic thickening of the vessel wall restricting the flow of blood through the lumen of the artery. Advanced stage plaques can sometimes rupture forming a luminal thombus which will either completely occlude the flow of blood or detach as an embolism and cause a stroke or myocardial infarction. Certain pathogenic infections have also been linked to atherogenesis. P. gingivalis, the etiological agent of human periodontal disease has been demonstrated to accelerate atherosclerosis in mice deficient in apolipoprotein E.
MRI is an effective imaging tool for cardiologists in both research and the clinical setting that offers a high-resolution, non-invasive, and relatively safe imaging modality for diagnosis and study of atherosclerosis. In this thesis, we use MR angiography to investigate the serial progression of atherosclerosis in the innominate and subclavian arteries of mice deficient in apoE that were infected with a wild type P. gingivalis strain and a genetically modified strain in which the lipid A of the outer membrane was modified. Our findings show a serial trend of luminal narrowing in mice infected with the wild type strain while there was luminal dilation in mice infected with the lipid A mutant strain. Our data, though not statistically significant, suggests that mice infected with wild type P. gingivalis exhibit progressive atherosclerosis while those infected with the lipid A mutant P. gingivalis were not.
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