|  LAURA P. HALE, MD., PH.D.
The Hale laboratory employs techniques of cellular and molecular biology to study mechanisms responsible for the generation of both normal immune responses and immune-mediated diseases. Research in the laboratory is mainly focused on inflammatory bowel disease (IBD), an immune-mediated disorder that is hypothesized to result from the abnormal immune response of a genetically susceptible host to the antigens derived from enteric bacteria. Development of optimal treatments for disease requires a detailed understanding of mechanisms of disease pathogenesis. Thus current work in the laboratory is aimed at understanding triggers of intestinal inflammation and mechanisms of inflammation-associated neoplasia, in addition to developing novel therapies for IBD treatment. Ongoing research also includes investigating mechanisms that determine the immunogenicity of oral antigens, to develop novel adjuvants for oral vaccines. This work has relevance for pathogenesis and treatment of infectious diseases affecting the gastrointestinal tract, as well as for inflammatory bowel disease.
Dr. Hale is an expert in pathologic evaluation of colitis and immunodeficiency in both humans and mice and is board-certified in Anatomic and Clinical Pathology.
Selected Publications (2005 - 2009):
Chichlowski, M., Hale, L.P.: Effects of Helicobacter infection on research: the case for eradication of Helicobacter from rodent research colonies. Comp. Med., 59:10-17, 2009.
Chichlowski, M., Hale, L.P.: Bacterial-mucosal interactions in inflammatory bowel disease an alliance gone bad. Amer. J. Physiol., 295:G1139-G1149, 2008.
Onken, J.E., Greer, P.K., Calingaert, B., Hale, L.P.: Bromelain treatment decreases secretion of pro-inflammatory cytokines and chemokines by colon biopsies in vitro. Clin Immunol., 126:345-352, 2008.
Hale, L.P., Cianciolo, G.: Treatment of experimental colitis in mice with LMP-420, an inhibitor of TNF transcription. J. Inflamm., 5:4, 2008.
Fitzhugh, D.J., Shan, S., Dewhirst, M.W., Hale, L.P.: Bromelain treatment decreases neutrophil migration to sites of inflammation. Clin Immunol., 128:66-74, 2008.
Sharp, J.M., Vanderford, D.A., Chichlowski, M., Myles, M.H., Hale, L.P.: Helicobacter infection decreases reproductive success of IL-10-deficient mice. Comp Med., 58:447-453, 2008.
Chichlowski, M., Sharp, J.M., Vanderford, D.A., Myles, M.H., Hale, L.P.: Helicobacter typhlonius and H. rodentium differentially affect the severity of colon inflammation and inflammation-associated neoplasia in IL-10-deficient mice. Comp Med., 58:534-541, 2008.
Hale, L.P., Perrera, D., Gottfried, M.R., Maggio-Price, L., Srinivasan, S., Marchuk, D.A.: Neonatal infection with Helicobacter species markedly accelerates the development of inflammation-associated colonic neoplasia in IL-10-/- mice. Helicobacter, 12:598-604, 2007.
Hale, L.P., Fitzhugh, D.J., Staats, H.F.: Oral immunogenicity of the plant proteinase bromelain. Intl. Immunopharmacol., 6:2038-2046, 2006.
Hale, L.P., Greer, P.K., Trinh, C.T., Gottfried, M.R.: Treatment with oral bromelain decreases colonic inflammation in the IL-10-deficient murine model of inflammatory bowel disease. Clin Immunol. 116:135-142, 2005.
Hale, L.P., Greer, P.K., Trinh, C.T., James, C.L.: Proteinase activity and stability of natural bromelain preparations. Intl Immunopharmacol, 5:783-793, 2005.
Swidsinski, A., Weber, J., Loening-Baucke, V., Lochs, H., Hale, L.P.: Spatial organization and composition of the mucosal flora in inflammatory bowel disease. World J. Gastroenterol., 11;1131-1140, 2005.
Swidsinski, A., Weber, J., Loening-Baucke, V., Hale, L.P., Lochs, H.: Spatial organization and composition of the mucosal flora in patients with inflammatory bowel disease. J. Clin Microbiol. 43:3380-3389, 2005.
Hale, L.P., Gottfried, M.R., Swidsinski, A.: Piroxicam treatment of IL-10 deficient mice enhances colon epithelial apoptosis and mucosal exposure to intestinal bacteria. Inflamm. Bowel Dis. 11:1060-1069, 2005.
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