COVER IMAGE

As a research assistant, my work focused on elucidating the pathogenic role of bacterial surface antigens in lung colonization and infection. My studies also explored various conjugate vaccine approaches against chronic bacterial infections. At the time, there did not exist a mouse model that mimicked the major clinical phenotype of chronic Pseudomonas aeruginosa infection in cystic fibrosis. During my tenure as a Research Assistant, I served as the primary investigator on the chronic P. aeruginosa study and developed a novel mouse model of chronic bacterial lung infection in the context cystic fibrosis. 

• Coleman, F. T., Mueschenborn, S., Meluleni, G., Ray, C., Carey, V. J., Vargas, S. O., Cannon, C. L., Ausuel, F. M., & Pier, G. B. (2003). Hypersusceptibility of Cystic Fibrosis Mice to Chronic Pseudomonas aeruginosa Oropharyngeal Colonization and Lung Infection. Proceedings of the National Academy of Sciences, 100 (4), 1949-1954 

• Pier, G. B., Coleman, F., Grout, M., Franklin, M., & Ohman, D. E. (2001). Role of Alginate O-Acetylation in the Resistance of Mucoid Pseudomonas aeruginosa to Opsonic Phagocytosis. Infection and Immunity, 69 (3), 1895-1901 

• Pier, G. B., Boyer, D., Preston, M., Coleman, F. T., Llosa, N., Mueschenborn-Koglin, M., Theilacker, C., Goldenberg H., Uchin J., Priebe GP, Grout M, Posner M, Cavacini L. (2004). Human Monoclonal Antibodies to Pseudomonas aeruginosa Alginate That Protect Against Infection by both Mucoid and Nonmucoid Strains. Journal of Immunology, 173 (9), 5671-5678

Pulmonary Center, Boston University School of Medicine

HOST-PATHOGEN INTERACTIONS DURING PNEUMOCOCCAL PNEUMONIA

My doctoral thesis work focused on an immunological study of macrophage cell signaling and responsiveness during bacterial pneumonia.  In this study, I expanded our understanding of the molecular mechanisms governing innate immune responses in the airways during Streptococcus pneumoniae infection. I developed a novel line of investigation into the role of alveolar macrophage NF-𝜅B activation during S. pneumoniae lung infection and the underlying mechanisms that influence airway remodeling and inflammation.

• Coleman, F.T., Blahna, M.T., Kamata, H., Yamatmoto, K., Zabinski, M.C., Kramnik, I., Wilson, A., Kotton, D. N., Quinton, L. J., Jones, M.R., Pelton, S., and Mizgerd, J.P. (2017). The Capacity of Pneumococci to Activate Macrophage NF-B Determines Necroptosis and Pneumonia Severity. Journal of Infectious Diseases, 216(4), 425-435 

• Smith, N.M.S., Wasserman, G.A., Coleman, F.T., Hilliard, K.L., Yamamoto, K., Lipsitz, E., Malley, R., Dooms, H., Jones, M.R., Quinton, L.J., and Mizgerd, J.P. (2017). Regionally compartmentalized resident memory T cells mediate naturally acquired protection against pneumococcal pneumonia. Mucosal Immunology, 11, 220-235

• Hartmann N, McMurtrey C, Sorensen ML, Huber ME, Kurapova R, Coleman FT, Mizgerd JP, Hildebrand W, Kronenberg M, Lewinsohn DM, Harriff MJ. (2018). Riboflavin Metabolism Variation Among Clinical Isolates of Streptococcus pneumoniae Results in Differential Activation of MAIT Cells. Am J Respir Cell Mol Biol., 58(6), 767-776

Department of Pathology/Transfusion Medicine, Harvard Medical School

INFLAMMATION AND THE BONE MARROW MICROENVIRONMENT DURING SICKLE CELL DISEASE

My postdoctoral research focused on the effects of inflammation on the bone marrow microenvironment and hematopoietic stem cell biology in Sickle Cell Disease (SCD). SCD is a hereditary red cell disorder caused by a single point mutation in the β-globin gene, which results in the synthesis of abnormal hemoglobin (hemoglobin S) in red blood cells. The two main clinical manifestations of SCD are chronic hemolytic anemia and acute vaso-occlusive crises (VOCs), and they are the principal causes of hospitalization for SCD patients. However, not much is known about the effects on the bone marrow microenvironment, especially the bone marrow niche components (such as vascular and mesenchymal cells). Using the humanized sickle cell mouse strain (Townes mouse), I worked on developing mouse models to study the molecular mechanisms that regulate bone marrow pathology in SCD; and optimizing confocal imaging, flow cytometry, and primary cell culture techniques to characterize the sickle cell related defects on mesenchymal stromal cell (MSC) subsets and hematopoiesis and osteogenesis.