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2016 DEPARTMENT OF MEDICINE RESEARCH DAY Title of Poster: A Membrane Glycerolipid Protects Against Immune-Mediated Liver Inflammation via Mobilization and Migration of Myeloid-Derived Suppressor Cells Presenter: Ramesh Halder, PhD Division: Rheumatology ☒ Faculty ☐ Fellow ☐ Resident ☐ Post-doc Research Fellow ☐ Graduate Student ☐ Medical Student ☐Other Principal Investigator/Mentor: Ram R. Singh, M.D. Thematic Poster Category: Atherosclerosis Co-Investigators: Priti Prasad, Cynthia Tran Infections, Injury and Repair, Inflammation, Host Defense, Immunology, Hemostasis and Abstract A Membrane Glycerolipid Protects Against Immune-Mediated Liver Inflammation via Mobilization and Migration of Myeloid-Derived Suppressor Cells Ramesh Halder, Priti Prasad, Cynthia Tran, Ram Raj Singh Autoimmunity and Tolerance Laboratory, Division of Rheumatology, Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA 90095, USA Membrane lipids function as essential components of biological membranes, as signaling molecules, and as energy storage molecules. Phosphatidic acid (PA) is a vital membrane lipid that serves as a precursor for the synthesis of all acylglycerol lipids in the cell. PA serves as a lipid second messenger that modulates diverse intracellular signaling. PA participates in a wide range of cellular processes, including vesicular trafficking, cytoskeletal organization, secretion, endocytosis, exocytosis, cell proliferation, differentiation, migration and survival. Administration of large doses of PA in animals (1 mg per mouse) can increase serum levels of pro-inflammatory cytokines. PA can do so by stimulating the production of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6 in macrophages through the Akt and mTOR pathways. Thus, PA may play facilitate the initiation of the host inflammatory response. Here, we examined the effect of PA in an inflammatory condition. Contrary to the above reports, PA protected against immune mediated liver inflammation induced by concanavalin A and reduced pro-inflammatory cytokines but increased anti-inflammatory cytokine interleukin-10 in the liver. PA did so by inducing the mobilization and migration of monocytic myeloid-derived suppressor cells that upon adoptive transfer protected against autoimmune liver inflammation. Our novel observations indicating immune protective functions of PA may have wide implications for a variety of conditions with altered lipid metabolism and inflammation such as atherosclerosis and autoimmune disease and conditions with local or systemic alterations in PA such as osteoarthritis and Alzheimer’s disease. Acknowledgement: Supported by NHLBI R21 and NIAID R01 to RRS, NIAMS F31 to CT, RRF Preceptorship and Gina Finzi fellowship to PP.