Deborah Stearns-Kurosawa, PhD

Deborah Stearns-Kurosawa, PhD

Associate Professor of Pathology & Laboratory Medicine

BS, Pennsylvania State University
PhD, Cleveland State University

BUMC Research Profile

Current laboratory interests include:

  • Study of enteric Shiga toxin-producing E.coli (STEC) infection and the Shiga-like ribosome inactivating toxins from these bacteria. The prototypic strain is E.coli 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.  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).  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.
  • Study of B.anthracis (anthrax) infection in a clinically relevant animal model. 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.  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.  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.
  • Study of how other pathologic conditions contribute to septic responses. 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.  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.