Associate professor, Manitoba Health Research Chair Professor in Immunology,Department of Immunology, Department of Medical Microbiology,Faculty of Health Sciences, College of Medicine,University of Manitoba.Address:Department of Immunology, Faculty of Health Sciences, College of Medicine,University of Manitoba,750 McDermot Avenue,425 Apotex Centre,Winnipeg, Manitoba, R3E 0T5.Phone: 1-204-977-5659Fax: 1-204-789-3921Email: firstname.lastname@example.org
Parasitic diseases continue to be one of the major causes of mortality and morbidity around the world (particularly in developing countries) and afflict more people than any other infectious disease. Sadly, despite the high mortality and morbidity and enormous socio-economic impact of parasitic diseases, not much interest is shown in this area of research and parasitic diseases remain relatively neglected in terms of research investment. In Dr. Uzonna’s laboratory, we study two diseases caused by protozoan parasites namely: Leishmaniasis and African trypanosomiasis. We utilize cellular and molecular immunologic approaches to study host-pathogen interactions that result in susceptibility or resistance to these diseases. We have taken these two-prong (host and pathogen) approach because we believe "it takes two to tango" and that the outcome of infection is influenced by the intricate interactions between the host and the pathogen. The overarching question that we seek answer to is:“what host and parasite factors contribute to susceptibility or resistance following infection with Leishmania or African Trypanosome?” Two major host factors of particular interest to our laboratory are regulatory T cells and memory T cells. Some of the questions we ask are:•Do memory cells develop after infection with protozoan parasites? If they do, how are they generated and are they important in resistance following secondary exposure? •What causes the loss of acquired immunity in animals that effectively controlled their primary parasitic infection?•How can regulatory T cells be activated to prevent immune cell hyper-activation and the subsequent pathology associated with such activation?From the parasite's side, we are interested in parasite-derived factors that:•Enhance the invasion process resulting in establishment of infection•Contribute to the take-over of host immune defenses •Alter the host immune system to make it permissible for parasite proliferation (immunomodulation).We utilize a variety of animal models, including targeted gene knockout and transgenic mice, genetically modified parasites, and more recently, proteomics to dissect cellular immune responses following protozoan infections. Although we primarily use mouse models in our studies, we are working towards finding vaccines for humans and livestock. Some of our vaccine candidates are in the early/planning stages of conducting protection studies in non-human primates.If you are interested in finding a cure and/or vaccines against poverty-associated and neglected diseases of the developing world, come and join the dynamic and enthusiastic team of trainees and researchers in Dr. Uzonna’s Lab.
Welcome to Uzonna Lab
Another important research activity going on in ourlaboratory (Host-PathogenInteraction Laboratory) involves understanding the pathogenesis of Sepsis/Septic Shock. Sepsis syndrome (also known as systemic inflammatory response associated with infection, sepsis, severe sepsis, and septic shock) is a condition characterized by a whole-body inflammatory state and the presence of a known or suspected bacteria, usually gram-negative organisms. Sepsis syndrome and septic shock are common and frequently fatal clinical conditions in all age groups and are leading causes of mortality in intensive care units, particularly in children and older adults. Therefore, understanding the pathogenesis of the disease is an important step towards designing appropriate clinical interventions both for preventive and treatment purposes.We have successfully developed a laboratory model of lipopolysaccharide - induced acute inflammation leading to septic shock in mice. We have also developed an Escherichia coli-induced model of inflammation in mice. We are using both models to interrogate the role of regulatory T cells, a subset of T cells that act to restrain and/or suppress excessive immune activation, and phosphoinositide 3-kinase (PI3K), a key intracellular signalling enzyme, in ameliorating sepsis and acute inflammatory responses. There are ongoing clinical studies aimed at expanding autologous human regulatory T cells in vitro, for in vivoinfusion to treat autoimmune disorders. We envisage situations where this could also be done for the management of sepsis and septic shock in patients.