John C. Brown

My undergraduate work at Auburn University, Auburn, Alabama, led to a B.S. degree in Forestry in 1965. I stayed for a little while longer and received the M.S. degree in Plant Physiology in 1967 under the guidance of Dr.Mason C. Carter, while working on the metabolism of herbicides. After a stint in the Navy aboard the U.S.S. Guadalcanal (LPH-7) from 1967-1969, I returned to graduate school and received the Ph.D. in Biochemistry in 1973 from North Carolina State University, Raleigh, North Carolina under the guidance of Dr. H. Robert Horton. There, I worked on solid-phase proteolytic enzyme kinetics, and protein conformation. I then headed due West, and became a post-doctoral fellow for three years ('73 - '76) in the (then) Department of Bacteriology and Immunology, at the University of California, Berkeley, California, under the guidance of Dr. Marian E. Koshland. While with Dr. Koshland, I learned Immunology, and worked on conformational changes within antibody molecules that resulted from ligand:antibody binding-site interactions. After leaving Berkeley, I headed due East, and stopped about half-way back to North Carolina, in Lawrence, Kansas. I became an Assistant Professor of Microbiology at KU in 1976, and began my research on autoimmune diseases, with a focus upon autoantibody induction and specificity. I worked for many years on rheumatoid factor and monoclonal antibodies with rheumatoid factor-like binding specificity, then began a relatively long-term collaboration with Dr. Dean Stetler in the Department of Biochemistry here at KU through work on systemic lupus erythematosus (SLE). In recent years I have collaborated with Dr. Joseph Murray in investigations of Type I (insulin-dependent) diabetes exhibited by the NOD and NOD SCID mouse. I am currently collaborating with Dr. Mary Hise at the University of Kansas Medical Center to examine the immune status of patients on long-term total parenteral nutrition.

Research Interests

When people are severely injured or have extensive surgery that does not affect ingestion of solid or liquid food (nutrition), the person will be fed through the alimentary tract (mouth, esophagus, stomach, small bowel, large bowel, etc). Provision of nutrients via the alimentary tract is known as enteral nutrition. If the alimentary tract is impaired in any way or if parts of the tract including the bowels (small, large or both) are missing, nutrients must be provided via a vein (the subclavian vein). Receipt of all nutrients that are necessary for life (in the form of salts, amino acids, lipids, sugars and vitamins, etc.) is known as total parenteral nutrition, or, TPN. People who have for one reason or the other lost bowel function must receive TPN for as long as the person is alive. Patients who receive TPN for several months or longer are termed, long-term TPN patients. My research interests are currently focused upon the study of alterations in immune function of patients on long-term total parenteral nutrition (TPN). Persons who require long-term feeding via TPN may eventually suffer from frequent bouts of central line infections, osteoporosis and liver disease In collaboration with Dr. Mary Hise at the University of Kansas Medical Center, the goal of the research is to determine the mechanism by which feeding patients via the subclavian vein appears to alter immune function of the patient. While these dysfunctional events appear to be related to immune system dysfunction and/or imbalance, and/or inflammatory sequealae, the cause of these harmful conditions is not yet known. The research involves examination of patient immune profiles including assessment of activity of various cytokines, functional and flow cytometric analyses of the CD4+ and CD8+ T cell populations and, in vitro cellular responses of peripheral blood lymphocytes. Additionally, a mouse model for TPN treatment is under development. This model will allow manipulation of experimental parameters including TPN content, genetics of the mouse and expression of cellular molecules important to lymphocyte interaction. This experimental approach, combined with patient data, will allow determination of the mechanism by which long-term TPN treatment induces alteration of immune function. Determination of the mechanism(s) of this system will hopefully provide a clinical approach that will reduce or alleviate the conditions associated with long-term TPN treatment.

Some Publications
Rombach, E., D.A. Stetler, and J.C. Brown. 1993. Induction of an anti-Fab, anti-DNA, and, anti-RNA polymerase I autoantibody response network in rabbits immunized with SLE anti-DNA antibody. Clinical and Experimental Immunology 94: 466-472.

Brown, J.C. 1996. What the heck is mad cow disease?.In: Notices and News, pp.27-29; June Issue; Society for Applied Bacteriology, Harrod, United Kingdom.

Fullwood, S., T.A. Hicks, J.C. Brown, R.L. Norman, and J.J. McGlone. 1998. Floor space needs for laboratory mice: C57Bl/6 males in solid-bottom cages with bedding. ILAR Journal 39(1): 29-36.

Brown, J. 2001. Don't Touch That Doorknob! How Germs Can Zap You and How You Can Zap Back, Warner Books, 303 pp.

Murray, J. S., Jois, S.D.S., Schountz, T., Ford, S. R., Tawde, M. D., Brown, J. C., Siahaan, T. J. 2002. Modeling alternative binding registers of a minimal immunogenic peptide on two class II major histocompatibility complex (MHC-II) molecules predicts polarized T-cell receptor (TCR) contact positions. J. Pept. Res. 59:115-122

Brief Biographical Sketch
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