Abstract 12625: Splenic Leukocytes Defines the Resolution of Inflammation and Left Ventricle Healing in Heart Failure Pathology

• DOI: 10.1161/circ.134.suppl_1.12625
• Publication Date: 2024-04-23T10:55:56Z
• Authors: Ganesh V Halade; Iliyan Vlasakov; Vasundhara Kain; Paul Norris; Charles N Serhan; Kevin A Ingle

Introduction: After myocardial infarction (MI) self-healing is prominent in mice but not humans. MI-induced innate inflammatory and resolving response unclear left ventricle (LV) healing. Hypothesis: To define response, our aim was to quantitate time-dependent generation of specialized pro-resolving mediators (SPMs) leukocyte trafficking the LV spleen post-MI. Methods: We determined kinetics by flow cytometry quantitated resolution metabolome using mass spectrometry C57BL/6 after permanent coronary ligation. Results: Lipid Mediator metabololipidomic analyses revealed that only serves as a reservoir it also participates actively SPMs production Post-MI (CD11b + Ly6G CD206 ) turnover at d1 linked increased levels infarcted with marked increase resolvin (Rv)D1, RvD3-6, maresin (MaR)1, lipoxins (LX) protectin D1 compared d0 naïve controls d5 Before MI, such RvD5, RvD6, (PD)1, AT-PD1, MaR1, LXA 4 , AT-LXA AT-LXB were higher than indicating splenic leukocytes mobilize activate healing program Lipoxygenase (LOX -5, -12 -15) preferentially activated LV, while cyclooxygenase (COX-1 -2) comprehensive provided self-regulating means pro-inflammatory neutrophils macrophages Ly6C hi time dependent manner lesser extent spleen. Thus, storage SPMs, LOX-mediated COX-mediated prostanoids facilitates murine Conclusions: The abundance before MI amplified within 24 hours post-MI confirms determine acute phase coincides demands investigation role heart failure pathology.