Abstract 15066: Porphyromonas ginigivalis-Induced Atherosclerosis is Transferred by Bone Marrow Transplant
Periodontal disease (PD) is a destructive inflammatory disease of the periodontium and Porphyromonas gingivalis (Pg) is a keystone pathogen in its early onset. Mounting evidence supports a role for PD as an independent risk factor for atherosclerosis. In human studies, after successful PD treatment, cardiovascular disease event risk is not decreased, suggesting that PD risk persists after pathogen elimination. This may be due to long term changes in immune cells and their precursors. In PD and atherosclerosis, macrophages are the important disease-causing immune cells. Our previous work showed that PD in an atherosclerosis mouse model significantly increased lesion burden.The aim of this study was to determine if increased atherosclerosis as a result of PD is transferred by immune precursor cells from the bone marrow (BM).Using the Low Density Lipoprotein Receptor Knock-out (LDLRo) mouse model of atherosclerosis, we transplanted BM from mice with western diet-induced atherosclerosis that were either infected with Pg or sham treated, to naïve LDLRo mice. At study midpoint, we collected blood for cholesterol and cytokine analyses. After 16 weeks, we collected blood and dissected, stained and scanned the aortas for en face morphometric analysis using Adobe Photoshop, software.Our results showed that mice receiving BM from donors experimentally infected with Pg had significantly greater atherosclerotic lesion burden compared with mice receiving BM from sham infected mice. In male mice, pro-inflammatory cytokines; G-CSF, C5/C5a and TREM-1 were 1-5 fold higher in mice receiving BM from donors experimentally infected with Pg. Importantly, there were no differences in weight, blood glucose or cholesterol levels between the groups.Our results suggest that increased atherosclerosis as a result of PD can be transferred by BM immune precursor cells, and that the systemic long term PD effect may in part be due to changes induced in the BM. These changes might be epigenetic modifications in inflammatory genes which we are currently studying.
Author Disclosures: M. Omar: None. M. Alexiou: None. M. Febbraio: None.
- © 2016 by American Heart Association, Inc.