Filip Swirski, PhD
- PROFESSOR | Medicine, Cardiology
- PROFESSOR | Diagnostic, Molecular and Interventional Radiology
Research Topics:Alzheimer's Disease, Autoimmunity, B Cells, Blood, Brain, Cardiac Arrest and Resuscitation, Cardiovascular, Cellular Immunity, Chemokines, Chemotaxis, Cytokines, Dendritic Cells, Endocrinology, Hematopoiesis, Immunology, Inflammation, Lung, Lymphocytes, Macrophage, Microglia, Pathology, Sleep Medicine, Stem Cells, Stress, Systems Biology, T Cells, Transgenic Mice, Viruses and Virology
Dr. Swirski obtained his PhD at McMaster University in Canada and postdoctoral studies at Brigham and Women’s Hospital. Dr. Swirski was Professor at Harvard Medical School and Massachusetts General Hospital before joining Mount Sinai in 2021. Dr. Swirski’s research focuses on innate immunity and inflammation in cardiovascular disease. He uses in vivo models of acute and chronic inflammation relevant to cardiovascular and metabolic diseases, with specific emphasis on cell development, communication, and function. Recently, his focus has expanded to include lifestyle factors such as sleep, diet, and stress as critical modulators of cardiovascular health and hematopoiesis.
Multi-Disciplinary Training AreasImmunology [IMM], Microbiology [MIC], Neuroscience [NEU]
PhD, McMaster University
Harvard Medical School
ESC William Harvey Lecture on Basic Science
Tucker Collins Lecture
Leaders in Cardiovascular Science Profile
Jeffrey M Hoeg Award for Basic Science and Clinical Research
Established Investigator Award
Patricia and Scott Eston MGH Research Scholar
Martin Prize for Fundamental Research
Outstanding Investigator Award
Howard M. Goodman Fellowship
Systemic Inflammatory Networks and Inter-Organ Communication
Systemic inflammatory networks connect various cardiovascular and metabolic processes. I showed that the spleen produces monocytes by extramedullary hematopoiesis. I provided evidence for the relative contribution of monocyte recruitment and macrophage proliferation atherosclerosis. I identified an on-demand mechanism by which transient monocyte-derived macrophages dispose of erythrocytes and recycle iron. I identified a population of intraepithelial T cells that modulate dietary metabolism and contribute to cardiovascular disease.
Monocytes and Macrophages in Cardiovascular Disease
A major long-standing focus is to understand how monocytes and macrophages participate in atherosclerosis and myocardial infarction. I showed that monocytes accumulate continuously in evolving atherosclerotic lesions. I linked atherosclerosis with blood monocytosis. I identified a biphasic monocyte-macrophage response that coordinates healing, and discovered a monocyte reservoir in the spleen. I showed that sleep protects against atherosclerosis by limiting monocyte production.
Hematopoiesis and Growth Factors
Survival, proliferation, and differentiation of hematopoietic cells it tightly controlled by various cell-specific factors. I discovered a GM-CSF-producing B cell that protect against sepsis and pneumonia. I showed that the growth factor IL-3 aggravates sepsis by eliciting the cytokine storm. I defined a critical role for IL-3 in myocarditis. I demonstrated that T cell output in the thymus relies on liver X receptors.