Glycolytic reprogramming fuels myeloid cell-driven hypercoagulability
Aisling M. Rehill, Gemma León, Seán McCluskey, Ingmar Schoen, Yasmina Hernandez-Santana, Stephanie Annett, Paula Klavina, Tracy Robson, Annie M. Curtis, Thomas Renné, Séamus Hussey, James S. O’Donnell, Patrick Walsh, Roger J. S. Preston
Abstract
BACKGROUND: Myeloid cell metabolic reprogramming is a hallmark of inflammatory disease; however, its role in inflammation-induced hypercoagulability is poorly understood. OBJECTIVES: We aimed to evaluate the role of inflammation-associated metabolic reprogramming in regulating blood coagulation. METHODS: We used novel myeloid cell-based global hemostasis assays and murine models of immunometabolic disease. RESULTS: innate myeloid cells within inflamed colonic tissue that were absent from the intestinal tissue of healthy mice. CONCLUSION: Collectively, this study identifies immunometabolic regulation of myeloid cell hypercoagulability, opening new therapeutic possibilities for targeted mitigation of thromboinflammatory disease.