Abstract P1043: Myocardial Infarction Induces Translocation Of Gut Bacteria To The Heart

Abstract

Introduction: Myocardial hypoxia & intestinal hyperpermeability (IH) are two important events commonly observed in the aftermath of a myocardial infarction (MI) event. Recent studies have shown that gut bacteria and their metabolites are able to leak into the systemic circulation due to post-MI IH. Hypothesis: We hypothesized that facultative anaerobic gut bacteria such as E. coli will be able to translocate and colonize the hypoxic heart post-MI. Methods: C57 mice were given an oral administration of 10e9 cfu of luciferase/GFP expressing E. coli Nissle (EcN). Permanent occlusion of LAD arteries was performed to induce MI. Mouse hearts were checked for presence of EcN using PCR at different timepoints (n=32), IHC (n=4), and siderophore-based PET imaging (n=2). Immunoblotting of heart tissue lysate was used to check for presence of GFP. Results: PCR amplification of DNA extracted from MI hearts of mice given oral EcN revealed cardiac presence of translocated EcN. IHC analysis further confirmed presence of EcN in the heart. Siderophore-based PET imaging & radionuclide-based biodistribution studies revealed significantly higher uptake in the MI heart vs. Sham corroborating EcN presence. Immunoblotting revealed presence of GFP in cardiac tissue of MI mice suggesting that bacterial products and proteins could potentially translocate through the gut-heart axis. Conclusion: MI induced IH & myocardial hypoxia contribute to the translocation of gut bacteria and colonization of the ischemic heart.