Scott Fulton, MD
Assistant Professor of Medicine
Phone: (216) 368-8900
Fax: (216) 368-2034
E-mail: sxf24@case.edu
Education
MD - Wayne State University School of Medicine, 1989
Residency- Case Western Reserve University/ University Hospitals of Cleveland, 1992
Fellowship- Case Western Reserve University/University Hospitals of Cleveland, 1995
Research
My research is conducted in collaboration with W. H. Boom. M.D. We utilize a murine model of aerogenic M. bovis-BCG infection as a model for studying human tuberculosis and granuloma formation (Fulton, S. A. et al. Am. J. Resp. Cell Mol. Biol. 22, pp. 333-334, 2000). We study both innate and T cell mediated immune responses to determine why the lung is susceptible to persistent mycobacterial infection. Recently, we have been studying alveolar macrophages to determine if they enhance the susceptibility of the lung to mycobacterial infection. We have determined that BCG infection inhibits the antigen presenting function of alveolar macrophages thereby promoting survival of mycobacteria in the lung (Fulton, S. A., et. al. 2004 Infect. Immun. [in press]). With this model, growth of M. bovis-BCG, cytokine expression, immune cell activation and histopathology are examined using a variety of immunologic, bacteriologic, flow cytometric and histologic techniques.
In my laboratory, I also have initiated three new areas of research aimed at understanding how the lung modulates immune responses to M. bovis-BCG.
Program #1: Determine the role of bronchoalveolar antibody expression in the pathogenesis of M. bovis-BCG infection. We are currently focusing on using bronchoalveolar IgA antibody to identify unique mycobacterial antigens expressed in the lung. Our approach involves detection of IgA reactive antigens, mass spectrometry to determine the antigen's protein sequence, and the M. tuberculosis genome to identify the corresponding mycobacterial genes. We propose to clone and express new myco-bacterial proteins and evaluate their immunogenicity and efficacy as subunit vaccines.
Program #2: Determine the role of pulmonary surfactant proteins on the pathogenesis of M. bovis-BCG infection. Since pulmonary surfactant proteins may enhance phagocytosis of mycobacteria and modulate cytokine expression, we have initiated studies to determine if altered surfactant protein expression exacerbates disease or enhances protective immunity. In addition, we are utilizing an in vitro model to study immunologic functions of type II pneumocytes which line alveoli and are the principal source of pulmonary surfactant protein expression.
Program #3: Determine the ability of extracellular matrix (ECM) proteins to modulate macrophage and T cell functions in the lung. Since macrophages and T cells migrate in and out of the lung and contact ECM, we hypothesize that exposure of inflammatory cells to ECM down-modulates inflammation thereby protecting the lung from exuberant potentially damaging inflammation.
NIH Biosketch
Selected References:
• Fulton, S. A., Johnsen, J. M., Wolf, S., Sieburth, D. S. and W.H. Boom. 1996. IL-12 production by human monocytes infected with Mycobacterium tuberculosis : Role of phagocytosis. Infect. Immun. 64:2523-2531.
• Fulton S. A., Martin, T.D., Redline, R. W. and Boom, W. H. 2000. Pulmonary immune responses during primary Mycobacterium bovis-Calmetter-Guerin Bacillus infection in C57Bl/6 mice. Amer. J. Resp. Cell Mol. Biol. 22: 333-343.
• Fulton, S. A., Reba, S. M., Martin, T. D., and W. H. Boom. 2002. Neutrophil mediated mycobacteriocidal immunity in the lung during Mycobacterium bovis-BCG infection in C57Bl/6 mice. Infect. Immun. 70: 5322- 5327.
• Fulton, S. A. Reba, S. M., Pai, R. K., Pennini, M. Torres, M., Harding, C. V. and W. H. Boom. 2004. Inhibition of MHC-II expression and antigen processing in murine alveolar macrophages by M. bovis-BCG and the 19kDa mycobacterial lipoprotein. Infect. Immun. (in press)
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