Mycobacterium bovis Bacille-Calmette-Guérin Infection Aggravates Atherosclerosis
Autor: | Anissa Moussa, Moises A. Huaman, Stephanie Schmidt, Eddy S. Konaniah, George S. Deepe, Ravi K. Komaravolu, Joseph E. Qualls, David Y. Hui, Carl J. Fichtenbaum, David G. Kuhel, Shinsmon Jose |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
lcsh:Immunologic diseases. Allergy T cell Immunology T cells Inflammation 030204 cardiovascular system & hematology mycobacterium 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Cytotoxic T cell Oil Red O Immunology and Allergy Original Research Mycobacterium bovis biology business.industry Cholesterol biology.organism_classification 030104 developmental biology medicine.anatomical_structure chemistry tuberculosis inflammation LDL receptor medicine.symptom Bacille-Calmette-Guérin atherosclerosis monocytes business lcsh:RC581-607 Lipoprotein |
Zdroj: | Frontiers in Immunology, Vol 11 (2020) Frontiers in Immunology |
ISSN: | 1664-3224 |
DOI: | 10.3389/fimmu.2020.607957 |
Popis: | Tuberculosis has been associated with increased risk of atherosclerotic cardiovascular disease. To examine whether mycobacterial infection exacerbates atherosclerosis development in experimental conditions, we infected low-density lipoprotein receptor knockout (Ldlr-/-) mice with Mycobacterium bovis Bacille-Calmette-Guérin (BCG), an attenuated strain of the Mycobacterium tuberculosis complex. Twelve-week old male Ldlr-/- mice were infected with BCG (0.3–3.0x106 colony-forming units) via the intranasal route. Mice were subsequently fed a western-type diet containing 21% fat and 0.2% cholesterol for up to 16 weeks. Age-matched uninfected Ldlr-/- mice fed with an identical diet served as controls. Atherosclerotic lesions in aorta were examined using Oil Red O staining. Changes induced by BCG infection on the immunophenotyping profile of circulating T lymphocytes and monocytes were assessed using flow cytometry. BCG infection increased atherosclerotic lesions in en face aorta after 8 weeks (plaque ratio; 0.021±0.01 vs. 0.013±0.01; p = 0.011) and 16 weeks (plaque ratio, 0.15±0.13 vs. 0.06±0.02; p = 0.003). No significant differences in plasma cholesterol or triglyceride levels were observed between infected and uninfected mice. Compared to uninfected mice, BCG infection increased systemic CD4/CD8 T cell ratio and the proportion of Ly6Clow non-classical monocytes at weeks 8 and 16. Aortic plaque ratios correlated with CD4/CD8 T cell ratios (Spearman’s rho = 0.498; p = 0.001) and the proportion of Ly6Clow non-classical monocytes (Spearman’s rho = 0.629; p < 0.001) at week 16. In conclusion, BCG infection expanded the proportion of CD4+ T cell and Ly6Clow monocytes, and aggravated atherosclerosis formation in the aortas of hyperlipidemic Ldlr-/- mice. Our results indicate that mycobacterial infection is capable of enhancing atherosclerosis development. |
Databáze: | OpenAIRE |
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