Journal
SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-88479-y
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Funding
- Transatlantic Network of the Fondation Leducq
- Sergei Zlinkoff Fund
- NIH [U01 AI22285, R01 HL084312, K23 HL152013]
- Glorney-Raisbeck Fellowship Award in Cardiovascular Disease through the New York Academy of Medicine
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The study found that antibiotic-induced perturbation of the microbiome in a murine model of atherosclerotic plaque inflammation resolution may weaken the effectiveness of lipid-lowering in reducing the content of plaque inflammatory CD68-expressing cells.
Since alterations in the intestinal microbiota may induce systemic inflammation and polarization of macrophages to the M1 state, the microbiome role in atherosclerosis, an M1-driven disease, requires evaluation. We aimed to determine if antibiotic (Abx) induced alterations to the intestinal microbiota interferes with atherosclerotic plaque inflammation resolution after lipid-lowering in mice. Hyperlipidemic Apoe(-/-) mice were fed a western diet to develop aortic atherosclerosis with aortas then transplanted into normolipidemic wild-type (WT) mice to model clinically aggressive lipid management and promote atherosclerosis inflammation resolution. Gut microbial composition pre and post-transplant was altered via an enteral antibiotic or not. Post aortic transplant, after Abx treatment, while plaque size did not differ, compared to Apoe(-/-) mice, Abx(-) WT recipient mice had a 32% reduction in CD68-expressing cells (p=0.02) vs. a non-significant 12% reduction in Abx(+) WT mice. A trend toward an M1 plaque CD68-expresing cell phenotype was noted in Abx(+) mice. By 16S rRNA sequence analysis, the Abx(+) mice had reduced alpha diversity and increased Firmicutes/Bacteroidetes relative abundance ratio with a correlation between gut Firmicutes abundance and plaque CD68-expressing cell content (p<0.05). These results indicate that in a murine atherosclerotic plaque inflammation resolution model, antibiotic-induced microbiome perturbation may blunt the effectiveness of lipid-lowering to reduce the content of plaque inflammatory CD68-expressing cells.
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