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David M. Engman, MD, PhDAssociate Professor
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To visit the Engman Lab website click here.
Our laboratory is engaged in two different lines of investigation:
Molecular Parasitology. Trypanosomes are single-celled parasites that cause human illnesses such as sleeping sickness and Chagas' disease. These organisms have complex life cycles involving both insect and mammalian hosts. The American trypanosome, Trypanosoma cruzi, is transmitted by reduviid bugs and evades the host immune response by penetrating host cells and differentiating into a form that replicates within the host cell cytoplasm. Transitions between the insect vector and the mammalian host are accompanied by complex morphologic and biochemical changes affecting virtually every part of the parasite cell. We are interested in the biogenesis of the mitochondria and flagella in these unique eukaryotic organisms, since these organelles are essential for cell survival as well as targets for the development of antiparasitic drugs.
Molecular Cardiology. 20 million Latin Americans are infected with T. cruzi and approximately 30 percent suffer from Chagas' heart disease. We are testing the hypothesis that immune responses directed toward both parasite antigens and heart antigens (i.e., autoimmunity) contribute to pathogenesis and have developed a mouse model of infection that exhibits both features. Mice develop severe myocarditis several weeks after infection that possesses all of the key features of the human disease, including strong parasite-specific and heart-specific humoral and cellular immunity. The overall objectives of these studies are (I) to elucidate the mechanisms by which parasite infection leads to cardiac inflammation, (ii) to determine the mechanisms by which autoreactive T cells are induced to proliferate and cause heart disease and (iii) to develop novel, immunomodulatory therapies for the treatment of myocarditis.
McGwire, B. S., Chang, K.-P. and Engman, D. M. (2003) Migration through the extracellular matrix by the parasitic protozoan Leishmania is enhanced by surface metalloprotease GP63. Infect. Immun. 71, 1008-1010.
Leon, J.S., Wang, K. and Engman, D.M. (2003) Captopril ameliorates myocarditis in acute experimental Chagas disease. Circulation 107, 2264-2269.
McGwire, B.S., Olson, C.L., Tack, B.F. and Engman, D.M. (2003) Killing of African trypanosomes by antimicrobial peptides. J. Infect. Dis. 188, 146-152.
Godsel, L.M., Leon, J.S., Wang, K., Fornek, J.L., Molteni, A. and Engman, D.M. (2003) Captopril prevents experimental autoimmune myocarditis. J. Immunol. 171, 346-352.
Leon, J.S., Wang, K. and Engman, D.M. (2003) Myosin autoimmunity is not essential for cardiac inflammation in acute Chagas disease. J. Immunol. 171, 4271-4277.
Leon, J.S., Daniels, M.D., Toriello, K.M., Wang, K. and Engman, D.M. (2004) A cardiac myosin-specific autoimmune response is induced by immunization with Trypanosoma cruzi proteins. Infect. Immun. 72, 3410-3417.
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View Publications by David Engman listed in the National Library of Medicine (PubMed). |
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