{"id":1921,"date":"2011-02-16T15:57:26","date_gmt":"2011-02-16T20:57:26","guid":{"rendered":"https:\/\/www.bumc.bu.edu\/busm-pathology\/?page_id=1921"},"modified":"2019-09-04T16:31:07","modified_gmt":"2019-09-04T20:31:07","slug":"deborah-j-stearns-kurosawa-phd","status":"publish","type":"page","link":"https:\/\/www.bumc.bu.edu\/busm-pathology\/home\/people_main\/deborah-j-stearns-kurosawa-phd\/","title":{"rendered":"Deborah J. Stearns-Kurosawa, PhD"},"content":{"rendered":"

Associate Professor
\nAssociate Provost\/Dean ad interim<\/em> for Graduate Medical Sciences<\/p>\n

Contact Information<\/strong><\/h3>\n

Email: dstearns@bu.edu<\/a><\/p>\n

Research Interests<\/strong><\/h3>\n
\"dsk01\"<\/a>
Renal epithelial Vero cells (blue nucleus) with internalized Shiga toxin-type 2 (green) and anti-toxin peptide (red). The peptide redirects toxin to the lysosomal degradation pathway to protect cells. Experiment and imaging by Caitlin Leibowitz, graduate student.<\/figcaption><\/figure>\n

Why is it that some people get a bacterial infection, feel lousy for a few days, take antibiotics and then forget about it when they go back to class or work, but other people get the same infection and die in two weeks in the intensive care unit? It\u2019s all about what pathogen is invading and how our bodies respond to the infection.\u00a0 It\u2019s a highly orchestrated response that requires input from our immune, coagulation, neurologic, and inflammatory pathways.\u00a0 And this in turn requires coordinated responses from cells and molecules in each of these pathways.\u00a0 If the response is too much or inadequate, then \u00a0disintegration can lead to multiple organ failure, shock and death.\u00a0 We have multiple NIH-funded projects to identify contributions at the host, organ, cellular, molecular and genetic level that contribute to different responses to infection.\u00a0 We want to identify the point where this disintegration process remains reversible, so that patients can be identified earlier with better prognosis and less morbidity. \u00a0\u00a0Current laboratory interests include:<\/p>\n

    \n
  • Study of enteric Shiga toxin-producing E.coli (STEC) infection and the Shiga-like ribosome inactivating toxins from these bacteria.<\/em> The prototypic strain is E.coli<\/em> O157:H7, a persistent global public health problem. Antibiotics make the disease worse and STEC infection is the leading cause of acute kidney failure in young children in the US.\u00a0 We are developing clinically-relevant animal models to test therapeutics that work in the blood stream, in the intestinal tract and inside cells where the bacterial toxins invade (see Figure).\u00a0 Related projects include study of toxin distribution mechanisms in murine models, toxin-induced cellular stress responses, gene profiling of cellular responses to toxins, mathematical modeling of physiologic responses, and vaccine studies.<\/li>\n
  • Study of B.anthracis (anthrax) infection in a clinically relevant animal model.<\/em> Our laboratory altered the anthrax disease paradigm by demonstrating the critical contribution of the host septic response to the lethality of anthrax infection and showed how adjunctive therapeutics can be beneficial.\u00a0 Model characterizations include physiology changes, metabolic indicators, biomarkers of coagulation, inflammation and innate immunity, and antigen-specific B cell responses after challenge with bacteria, toxins or spores.\u00a0 Therapeutics are studied at different disease stages and vaccine approaches are evaluated and validated in the primate models for application in both civilian and military populations.<\/li>\n
  • Study of how other pathologic conditions contribute to septic responses.<\/em> One school of thought is that the decades of failed clinical trials to treat severely septic patients may be because research models have not taken into account co-morbidity contributions. Patients often are burdened with multiple problems, like obesity, diabetes and\/or autoimmune disease, at the time they get a severe bacterial infection.\u00a0 Each of these health problems have their own set of contributions to the pathways that respond to bacterial infection, and very little is known about how networked responses are altered accordingly.<\/li>\n<\/ul>\n

    Representative Publications<\/strong><\/h3>\n
      \n
    • Stearns-Kurosawa, DJ, Osuchowski MF, Valentine C, Kurosawa S, Remick DG.\u00a0 The Pathogenesis of Sepsis. Annu Rev Pathol Mech<\/em> Dis 6:19-48, 2011.\u00a0 Epub ahead of print 21Sept 2010 (PMID: 20887193).<\/li>\n
    • Stearns-Kurosawa, DJ, Collins V, Freeman S, Tesh VL, Kurosawa S.\u00a0 Distinct Physiologic and Inflammatory Responses Elicited in Baboons after Challenge with Shiga Toxin Type 1 or 2 from Enterohemorrhagic Escherichia coli.\u00a0 Infect Immun<\/em> 78(6):2497-2504, 2010.\u00a0 (PMID: 20308301<\/li>\n
    • Kinasewitz G, Stearns-Kurosawa DJ, Kurosawa S.\u00a0 Soluble Thrombomodulin: a sign of bad times.\u00a0 Crit Care Med<\/em>, 36(3):985-7, 2008. (PMID: 18431290<\/li>\n
    • Stearns-Kurosawa DJ, Lupu F, Taylor FB Jr, Kinasewitz G, Kurosawa S. Sepsis and pathophysiology of anthrax in a non-human primate model.\u00a0 Am J Pathol<\/em>, 169:433-444, 2006 (PMID: 16877346).<\/li>\n
    • Kaneko T, Stearns-Kurosawa DJ, Taylor, Jr. F, Twigg M, Osaki K, Kinasewitz GT, Peer G, Kurosawa S.\u00a0 Down-modulation of neutrophil CD10 expression in non-human primates and humans after in vivo<\/em> septic challenge.\u00a0 SHOCK<\/em> 20:130-137, 2003 (PMID: 12865656).<\/li>\n<\/ul>\n

      \n","protected":false},"excerpt":{"rendered":"

      Associate Professor Associate Provost\/Dean ad interim for Graduate Medical Sciences Contact Information Email: dstearns@bu.edu Research Interests Why is it that some people get a bacterial infection, feel lousy for a few days, take antibiotics and then forget about it when they go back to class or work, but other people get the same infection and […]<\/p>\n","protected":false},"author":1131,"featured_media":0,"parent":3281,"menu_order":45,"comment_status":"closed","ping_status":"closed","template":"","meta":[],"_links":{"self":[{"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/pages\/1921"}],"collection":[{"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/users\/1131"}],"replies":[{"embeddable":true,"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/comments?post=1921"}],"version-history":[{"count":8,"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/pages\/1921\/revisions"}],"predecessor-version":[{"id":15700,"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/pages\/1921\/revisions\/15700"}],"up":[{"embeddable":true,"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/pages\/3281"}],"wp:attachment":[{"href":"https:\/\/www.bumc.bu.edu\/busm-pathology\/wp-json\/wp\/v2\/media?parent=1921"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}