Dr. Russell assumed his position as Professor and Chair of the Department of Microbiology and Immunology in July 2000. He stepped down from his Chair's position in 2010 and now concentrates on his research work. His previous experience was as professor in the Department of Molecular Microbiology at Washington University School of Medicine, in St. Louis, where he had worked since 1990. He received a B.Sc. degree in Zoology from St. Andrews University in Scotland in 1979 and was awarded a Ph.D. from Imperial College, London University in 1982. He has held positions at the University of Kent, the Max-Planck-Institute in Tuebingen, and NYU School of Medicine prior to moving to St. Louis. His research program continues to be supported by funding from the National Institutes of Health for research into the biology of Mycobacterium and the role of the macrophage in infection.
Tuberculosis: The success of Mtb as a pathogen depends on the ability of the bacterium to survive and persist within the host macrophage. We are actively engaged in studying the behavior of both partners in this intimate relationship. On the macrophage side of the equation the lab has been developing real-time, functional readouts for the lumenal environment within the phagosome, such as hydrolytic activity and radical production, and determining these are modified by immune stimuli and infection. On the bacterial side the group is interested in how the bacterium modifies its intracellular compartment to ensure its survival, and how the bacterium senses and responds metabolically to this changing environment. This information is being used as the foundation for high-throughput screens to identify small molecules that kill M. tuberculosis inside its host cell. A project pursued in collaboration with Calibr, San Diego. We are also collaborating with researchers at the University of Cape Town, South Africa, examining ways of enhancing drug action in vivo.
HIV: In addition to infecting CD4 lymphocytes, HIV also infects macrophages, where it sets up a chronic, long-lived infection capable of generating infectious virus. The lab is studying how human alveolar macrophages respond to HIV and how HIV infection of the macrophage directly influences the ability of the body to control other infections, such as tuberculosis. These human studies are pursued through a collaboration with the Malawi-Liverpool-Wellcome Trust Research Laboratories, Blantyre, Malawi.
Malaria: Cerebral malaria is predominantly a pediatric syndrome that is responsible for the majority of deaths due to malaria in sub-Saharan Africa. This is a new project in the lab that focuses on the role on monocytes and macrophages in driving the pathology that leads to death in cerebral malaria. This work is pursued as a collaboration with the Michigan State University International Center for Excellence in Malaria Research group in Blantyre, Malawi.
The research is supported by grants from the NHLBI and NIAID institutes of the National Institutes of Health, and by the Bill and Melinda Gates Foundation.
Jambo, K.C., Banda, D., Kankwatira, A., Sukumar, N., Allain, T., Heyderman, R.S., Russell, D.G., and Mwandumba, H.C. (2014) Small alveolar macrophages are infected preferentially by HIV and exhibit impaired phagocytic function. Mucosal Immunology. Sep;7(5):1116-26. PMID: 24472847
Sukumar, N., Tan, S., Aldridge, B. B., and Russell, D.G. (2014). Exploitation of Mycobacterium tuberculosis reporter strains to probe the impact of vaccination at sites of infection. PLoS Pathogens. 10(9): e1004394. PMID: 25233380
Russell, D.G., Lee, W., Tan, S., Sukumar, N., Podinovskaia, M., Fahey, R.J., and VanderVen, B. C. (2014) The sculpting of the Mycobacterium tuberculosis genome by host-derived pressures. Microbiol Spectr. 2(2). PMID: 25584198
VanderVen, B.C., Fahey, R.J., Lee, W., Liu, Y., Abramovitch, R.B., Memmott, C., Crowe, A.M., Eltis, L.D., Perola, E., Deininger, D.D., Want, T., Locher, C.P., and Russell, D.G. (2015). Novel inhibitors of cholesterol degradation in Mycobacterium tuberculosis reveal how the bacterium’s metabolism is constrained by the intracellular environment. PLoS Pathogens. 11(2): e1004679. PMID: 25675247