Chlamydia pneumoniae infection induces an unstable atherosclerotic plaque phenotype in LDL-receptor, ApoE double knockout mice
Autor: | R Ezzahiri, H. A. J. M. Kurvers, Frank R. M. Stassen, C.A. Bruggeman, M.M.L. van Pul, Peter J.E.H.M. Kitslaar |
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Rok vydání: | 2003 |
Předmět: |
DNA
Bacterial Male Apolipoprotein E Pathology medicine.medical_specialty Arteriosclerosis Aortic Diseases Matrix metalloproteinase Unstable plaques Lesion Mice Apolipoproteins E Chlamydia pneumoniae medicine Animals Receptor Chlamydophila Infections Aorta Mice Knockout Medicine(all) Chlamydia business.industry Fibrous cap area Fibrous cap Chlamydophila pneumoniae medicine.disease Antibodies Bacterial Immunohistochemistry Actins Phenotype Matrix metalloproteinases medicine.anatomical_structure Matrix Metalloproteinase 9 Receptors LDL LDL receptor Matrix Metalloproteinase 2 Surgery medicine.symptom Cardiology and Cardiovascular Medicine business |
Zdroj: | European Journal of Vascular and Endovascular Surgery. 26(1):88-95 |
ISSN: | 1078-5884 |
DOI: | 10.1053/ejvs.2002.1913 |
Popis: | Objectives: to study whether Chlamydia pneumoniae (Cpn) infection affects atherosclerotic plaque morphology in atherogenic (LDLr/ApoE −/− ) mice. Methods: in mice sacrificed 20 or 40 weeks after Cpn infection aortic arch sections were analysed for lesion and fibrous cap area and the presence of matrix metalloproteinases (MMP)-2 and -9. Results: all infected mice seroconverted, demonstrated Cpn DNA in their aortas on PCR and developed atherosclerotic plaques. Infection was not associated with changes in lesion area or type, but was associated with reduced the fibrous cap area and increased MMP-2 and -9 immunoreactivity. Conclusion: these findings suggest that Cpn infection may predispose to plaque instability. Eur J Vasc Endovasc Surg 26 , 88-95 (2003) |
Databáze: | OpenAIRE |
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