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David M. Engman, MD, PhD
Professor of Pathology
Professor of Microbiology-Immunology
Director, Medical Scientist (MD/PhD) Training Program
Ward 6-175
303 E. Chicago Avenue
Chicago, IL 60611
d-engman@northwestern.edu
http://www.engmanlab.northwestern.edu
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Phone: (312) 503-1288
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Clinical Pathology
Molecular Diagnostics
Medical School
University Iowa
Site of Residency
Northwestern University Medical School
Research Interests
Molecular Cell Biology of Tropical Parasitic Diseases. 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.
Pathogenesis and Treatment of Inflammatory Heart Disease. 20 million Latin Americans are infected with the American trypanosome Trypanosoma 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.
Selected Publications
Tyler KM, Luxton GW, Applewhite DA, Murphy SC, Engman DM. Responsive microtubule dynamics promote cell invasion by Trypanosoma cruzi. Cell Microbiol 7:1579-91, 2005.
Buchanan KT, Ames JB, Asfaw SH, Wingard JN, Olson CL, Campana PT, Araujo AP, Engman DM. A flagellum-specific calcium sensor. J Biol Chem 280:40104-11 2005.
Hyland KV, Leon JS Daniels MD, Giafis N, Woods LM, Bahk TJ, Wang K, Engman DM. Modulation of autoimmunity by treatment of an infectious disease. Infect. Immun. 75, 3641-3650, 2007
Fridberg A, Olson CL, Nakayasu ES, Tyler KM, Almeida IC, Engman DM. Sphingolipid synthesis is necessary for kinetoplast segregation and cytokinesis in Trypanosoma brucei. J Cell Sci 121, 522-535, 2008
Daniels MD, Hyland KV, Wang K, Engman DM. Recombinant cardiac myosin fragment induces experimental autoimmune myocarditis via activation of Th1 and Th17 immunity. Autoimmunity 41, 490-499, 2008.
Hyland KV, Asfaw SH, Olson CL, Daniels MD, Engman DM. Bioluminescent imaging of Trypanosoma cruzi infection. Int. J. Parasitol. 38, 1391-1400, 2008
Tyler KM, Fridberg A, Toriello KM, Olson CL, Cieslak JA, Hazlett TL, Engman DM. Flagellar membrane localization via association with lipid rafts. J. Cell Sci. 122, 859-866, 2009
Emmer BT, Souther C, Toriello KM, Olson CL, Epting CL, Engman DM. Identification of a palmitoyl acyltransferase required for protein sorting to the flagellar membrane. J. Cell Sci. 122, 867-874, 2009
View more Publications by David M. Engman, MD, PhD
listed in the National Library of Medicine (PubMed)
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