Dr. Fulton is an Instructor at Case Western Reserve University School of Medicine in the Division of Infectious Diseases. As a fellow, Dr. Fulton was supported by an institutional training grant supported by the NIAID and a training grant from the American Lung Association. He has been responsible for setting up a new animal model to study the immune response to tuberculosis and chosen to continue studying tuberculosis at CWRU because of its long and productive interest in in immunity to tuberculosis. The scholarly environment was initiated by Dr. J. Ellner who is the current PI for a multi-center collaborative Tuberculosis Research Unit. Dr. Fulton's mentors, Drs. W. H. Boom and F. P. Heinzel are interested in cellular immune responses to complex intracellular pathogens and have had significant success in training physician scientists. Other members include Dr. Z. Toossi, Dr. R. Wallis, Dr. C. Hirsch and Dr. R. Silver who contribute to the intellectual environment. Additional formal and informal interactions with scientists in Geographic Medicine (Dr. J. Kazura, Dr. C. King, Dr. E. Pearlman) will foster Dr. Fulton's training environment. Dr. Fulton now proposes addditional specialized training with the goal of becoming an independent physician scientist. He has set up a mouse model of aerogenic M. bovis-BCG infection as a model of human disease since M. bovis-BCG grows in the lung and elicits protective T cell responses that eradicate 99 percent of the bacteria. 1 percent of bacteria persist in a steady state infection characterized by granuloma formation and immune surveillance. In contrast, viulent M. tuberculosis leads to progressive infection. Since human pulmonary immune responses can be only partially and indirectly studied, animal models have provided a means for studying the unique susceptibilty of the lung. To analyze immune responses that characterize the susceptibility of the lung to mycobacteria, three aims are proposed:
Aim 1. To characterize the expression of chemokines and cytokines within the bronchoalveolar and lung microenvironments during early, maximal, and late immune activation phases of aerogenic M. bovis-BCG and M. tuberculosis infection.
Aim 2. To characterize mycobacterial antigen presentation and T cell activation within the bronchoalveolar and lung microenvironments during early, maximal and late immune activation phases of aerogenic M. bovis-BCG and M. tuberculosis infection.
Aim 3. To characterize the early pulmonary immune responses to aerogenic M. bovis-BCG and M. tuberculosis during local and systemic immunomodulation of cytokine and chemokine expression.
|Kuchtey, John; Fulton, Scott A; Reba, Scott M et al. (2006) Interferon-alphabeta mediates partial control of early pulmonary Mycobacterium bovis bacillus Calmette-Guerin infection. Immunology 118:39-49|
|Fulton, Scott A; Reba, Scott M; Pai, Rish K et al. (2004) Inhibition of major histocompatibility complex II expression and antigen processing in murine alveolar macrophages by Mycobacterium bovis BCG and the 19-kilodalton mycobacterial lipoprotein. Infect Immun 72:2101-10|
|Fulton, S A; Reba, S M; Martin, T D et al. (2002) Neutrophil-mediated mycobacteriocidal immunity in the lung during Mycobacterium bovis BCG infection in C57BL/6 mice. Infect Immun 70:5322-7|