John G. Nedrud, Ph.D.Professor Emeritus
2103 Cornell Rd.
Cleveland, OH 44106-7288
phone: (216) 368-1281
fax: (216) 368-0494
|1970||B.S., Chemistry, South Dakota School of Mines and Technology|
|1976||Ph.D., Molecular Biology/Immunology, University of California, Los Angeles, California|
|1976-1983||Postdoctoral Fellow and Research Associate, Cancer Research Center, University of North Carolina in Chapel Hill|
|1983-present||Faculty member, Institute of Pathology, Case Western Reserve University|
My major interest is the mucosal immunology of pathogenic micro-organisms. I work primarily with animal models of Helicobacter pylori (the gram negative bacterium which causes ulcers and is a risk factor for gastric cancer) and also have extensive experience using animal models for respiratory viruses. I have been using animal models to develop oral (gastrointestinal) and intranasal immunization protocols to achieve protection versus these micro-organisms. Cholera toxin has been shown to be a very potent adjuvant for enhancing mucosal immune responses and we are studying its mechanism of action as well as whether non-toxic derivatives still have adjuvant activity. I am also studying how the host response contribuites to the diseases asssocited with Helicobacter infections. Finally, my laboratory has generated IgA monoclonal antibodies versus pathogenic micro-organisms and studied their protective effects in vitro and in vivo.
Chintalacharuvu SR, Nagy NU, Sigmund N, Nedrud JG, Amm ME, Emancipator SN (2001) T cell cytokines determine the severity of experimental IgA nephropathy by regulating IgA glycosylation. Clin Exp Immunol 126, 326-333.
Arulanandam BP, Raeder RH, Nedrud JG, Bucher DJ, Le J, Metzger DW (2001) IgA immunodeficiency leads to inadequate Th cell priming and increased susceptibility to influenza virus infection. J Immunol 166, 226-231.
Nedrud JG, Blanchard SS, Czinn SJ (2002) Helicobacter pylori inflammation and immunity. Helicobacter 7 (Suppl 1), 24-29.
Garhart CA, Redline RW, Nedrud JG, Czinn SJ (2002) Clearance of Helicobacter pylori infection and resolution of postimmunization gastritis in a kinetic study of prophylactically immunized mice. Infect Immun 70, 3529-3538.
Kobayashi N, Bagheri N, Nedrud JG, Strieter RM, Tomino Y, Lamm ME, Emancipator SN (2003) Differential effects of Sendai virus infection on mediator synthesis by mesangial cells from two mouse strains. Kidney Int 64, 1675-1684.
Garhart CA, Nedrud JG, Heinzel FP, Sigmund NE, Czinn SJ (2003) Vaccine-induced protection against Helicobacter pylori in mice lacking both antibodies and interleukin-4. Infect Immun 71, 3628-3633.
Eisenberg JC, Czinn SJ, Garhart CA, Redline RW, Bartholomae WC, Gottwein JM, Nedrud JG, Emancipator SE, Boehm BB, Lehmann PV, Blanchard TG (2003) Protective efficacy of anti-Helicobacter pylori immunity following systemic immunization of neonatal mice. Infect Immun 71, 1820-1827.
Garhart CA, Heinzel FP, Czinn SJ, Nedrud JG (2003) Vaccine-induced reduction of Helicobacter pylori colonization in mice is interleukin-12 dependent but gamma interferon and inducible nitric oxide synthase independent. Infect Immun 71, 910-921.
O'Brien, D. P., Israel, D. A., Krishna, U., Romero-Gallo, J., Nedrud, J., Medof, M. E., Lin, F., Redline, R., Lublin, D. M., et al. (2006). The role of decay-accelerating factor as a receptor for helicobacter pylori and a mediator of gastric inflammation 10.1074/jbc.M601805200. J. Biol. Chem. M601805200.
Yamashita, M., Chintalacharuvu, S. R., Kobayashi, N., Nedrud, J. G., Lamm, M. E., Tomino, Y. and Emancipator, S. N. (2007). Analysis of innate immune responses in a model of IgA nephropathy induced by Sendai virus. Contributions to nephrology 157, 159-163.
Chintalacharuvu SR, Yamashita M, Bagheri N, Blanchard TG, Nedrud JG, Lamm ME, et al. T cell cytokine polarity as a determinant of immunoglobulin A (IgA) glycosylation and the severity of experimental IgA nephropathy. Clinical and Experimental Immunolgy. 2008;153(3):456-62. PMCID: 2527359.
Ding H, Nedrud JG, Wershil B, Redline RW, Blanchard TG, Czinn SJ. Partial Protection against Helicobacter pylori in the Absence of Mast Cells in Mice. Infect Immun. 2009;77(12):5543-50.