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| Research Interest: Gastrointestinal inflammation with specific interests in immune-epithelial cell interactions in H. pylori infection and inflammatory bowel disease. The ultimate goal of understanding the pathogenesis of these diseases is to enhance the design of therapies for the treatment or prevention of chronic gastrointestinal inflammation. Currently, Dr. Crowe is pursuing two main projects. The first project is investigating the mechanisms whereby oxidative stress regulates the expression of genes in gastric epithelial cells during infection with H. pylori. These studies entail a characterization of the role of AP endonuclease in redox-sensitive expression of IL-8 and other genes that control inflammation. In the second project, Dr. Crowe is using mouse models of gastric cancer to study the impact of inflammation and oxidative stress in the control of epithelial cell growth and differentiation. This model also has relevance to the pathogenesis of cancer associated with other forms of inflammation including ulcerative colitis and celiac disease. Representative PublicationsFan XJ, Crowe SE, Behar S, Gunasena H, Ye G, Haeberle H, Van Houten N, Gourley WK, Ernst PB, and Reyes VE: The effect of class II major histocompatibility complex expression on adherence of Helicobacter pylori and induction of apoptosis in gastric epithelial cells: a mechanism for T helper cell type 1-mediated damage. J. Exp. Med. 187(10):1659-1669, 1998. Casola, A., Estes, M.K., Crawford, S.E., Ernst, P.B., Garofalo, R. Ogra, P., Crowe, S.E. Rotavirus infection of cultured intestinal epithelial cells induces secretion of CXC and CC chemokines. Gastroenterology 114:947-955, 1998. Denning, T.L., Takaishi, H., Crowe, S.E., Boldogh, I., Jevnikar, A., and Ernst, P.B. Oxidative stress induces the expression of Fas and FasL and apoptosis in murine intestinal epithelial cells. Free Rad. Biol. Med. 33:1641-1650, 2002. Casola, A., Garofalo, R.P., Crawford, S.E., Estes, M.K., Mercurio, F., Crowe, S.E. Brasier, A.R., Interleukin-8 gene regulation in intestinal epithelial cells infected with rotavirus: role of viral-induced IkB kinase activation. Virology 298, 8-19; 2002. Smith, MF Jr., Mitchell A, Li G, Ding S, Fitzmaurice AM, Ryan K, Crowe, SE, Goldberg, JB. TLR2 and TLR5, but not TLR4, are required for Helicobacter pylori-induced NF-kappa B activation and chemokine expression by epithelial cells. J. Biol. Chem. 278, 32552-32560; 2003. |
