Education & Training
- Medical School – Georgetown University – MD
- Residency – University of Alabama – Internal Medicine
- Fellowship – University of Washington – Pulmonary/Critical Care Medicine
- Post-Doctoral Fellowship – University of Washington – Pulmonary/Critical Care Medicine
NIH Grants: R01, R21
Dr. Lee’s research interests stem from her clinical interest in the biology of the critical illness, and host determinants of lung injury from severe pneumonia. Her laboratory focuses upon effector function of innate immune cells of the myeloid lineage including macrophages and neutrophils that provide the initial host response to acute lung infection. Dr. Lee studies host-pathogen interactions utilizing relevant respiratory pathogens Pseudomonas aeruginosa and Klebsiella pneumoniae in model systems to understand the molecular basis of normal and aberrant host immune response. One area of focus is mechanisms of host protection mediated by the matricellular protein thrombospondin-1 secreted by vascular endothelium and platelets during inflammation. Dr. Lee has shown that thrombospondin-1 dampens pathogenic neutrophil responses during the acute phase of Pseudomonas aeruginosa-induced injury by limiting extracellular matrix proteolysis and triggers the production of the anti-inflammatory cytokine IL-10 by macrophages during the resolution phase of injury. Another focus of Dr. Lee’s laboratory is how the scavenger receptor CD36 is pivotal in the proximal control of macrophage effector cytokine responses and phagocytosis by amplifying type I and II interferon response against K. pneumoniae in the lungs. Dr. Lee’s laboratory utilizes a repertoire of relevant murine models of injury, molecular genetic approaches, in vitro biochemical assays, and human bio-samples to examine innate host defenses in privileged mucosal sites such as the lower respiratory tract. She is actively involved in research training and teaching of medical students, graduate students, residents and fellows in Pulmonary and Critical Care Medicine. Her educational interest primarily focuses on training the next generation of physician-scientists and scientists interested in innate immunity, inflammation, cellular and molecular pathology of the lung.
- McComb JG, Ranganathan M, Pilewski JM, Ray P, Watkins SC, Choi AM, Lee JS. CX3CL1 Upregulation is Associated with Recruitment of CX3CR1+ Mononuclear Phagocytes and T Lymphocytes in the Lungs during Cigarette Smoke Induced Emphysema. The American Journal of Pathology. 2008; October 173(4): 949-61.
- Mangalmurti NS, Xiong Z, Hulver M, Ranganathan M, Liu XH, Oriss T, Rubin M, Triulzi D, Choi A, Lee JS. Loss of Red cell Chemokine Scavenging Promotes Transfusion Related Lung Inflammation. Blood. 2009; January 29; 113(5): 1158-66.
- Mangalmurti NS, Chatterjee S, Chen GJ, Mohammed A, Anderson E, Siegel DL, Schmidt AM, Albelda SM, Lee JS. Advanced glycation endproducts on stored erythrocytes increase endothelial reactive oxygen species generation through interaction with RAGE. Transfusion. 2010; November; 50(11):.
- Mei J, Liu Y, Dai N, Favara M, Greene T, Jeyaseelan S, Poncz M, Lee JS, Worthen GS. CXCL5 regulates chemokine scavenging and pulmonary host defense to bacterial infection. Immunity. 2010; July 23;33(1): 106-17.
- Lee JS, Gladwin MT. Bad Blood: The Risks of Red Cell Storage. Bedside to Bench Invited Commentary. Nature Medicine. 2010; 16: 381–382.
- Xiong Z, Cavaretta J, Qu L, Stolz DB, Triulzi D, Lee JS. Red cell microparticles show altered inflammatory chemokine binding and release ligand upon interaction with platelets. Transfusion. 2010; 51(3): 610-621.
- Xiong Z, Leme AS, Ray P, Shapiro SD, Lee JS. CX3CR1+ Lung Mononuclear Phagocytes Spatially Confined to the Interstitium Produce TNF-Alpha and IL-6 and Promote Cigarette Smoke Induced-Emphysema. The Journal of Immunology. 2011; March 1;186(5): 3206-14.
- Zhao Y, Xiong Z, Lechner EJ, Chan Y, Zhang Y, Ross MA, Stolz DB, Rosengart MR, Pilewski J, Ray P, Ray A, Silverstein RL, Lee JS. Thrombospondin-1 triggers macrophage IL-10 production and promotes resolution of experimental lung injury. Mucosal Immunol. 2014; March;7(2): 440-8.
- Zhao Y, Olonisakin TF, Xiong Z, Hulver M, Sayeed S, Yu MT, Gregory AD, Kochman EJ, Chen BB, Mallampalli RK, Sun M, Silverstein RL, Stolz DB, Shapiro SD, Ray A, Ray P, Lee JS. Thrombospondin-1 regulates neutrophil microbial killing by restraining granule serine proteases during K. pneumoniae infection. Mucosal Immunol. 2014; December 10; 8(4): 896-905.
- Balasubramanian KK, Maeda A, Lee JS, Mohammadyani D, Tyurin VA, Tyurina YY, Ray P, Klein-Seetharaman J, Mallampalli RK, Bayir H, Fadeel B, Kagan VE. Extracellular Cardiolipins Are Phagocytized by Macrophages and Silence LPS Signaling by Mimicking Immature Lipid A. Science Signal. 2015; September 22;8(395):.