Charles O. Elson, III, MD, Professor

 


rsz_dr_elson_2013


         
Dr.Elson received his M.D. from Washington University in St. Louis, trained in Internal Medicine at New York Hospital/Cornell, then did his Gastroenterology fellowship at the University of Chicago.  After doing full-time research in immunology at N.I.H., he joined the Faculty of the Division of Gastroenterology at the Medical College of Virginia.  He moved to the University of Alabama at Birmingham to become Director of the Division of Gastroenterology and Hepatology,  and subsequently served as Vice-Chair for Research in the Department of  Medicine.  He holds the Basil I. Hirschowitz Chair in Gastroenterology and is an active consultant in immune-mediated intestinal disorders.

The author of numerous peer-reviewed manuscripts, reviews, and book chapters, Dr. Elson as held major positions in national organizations, and has served on a number of advisory boards, including the Advisory Council of the National Institute of Diabetes and Digestive and Kidney Diseases.  He has been elected to many of the most outstanding professional societies in the field of academic medicine and has a long history of service to the Society for Mucosal Immunology for which he is a co-founder and past president.

Dr.Elson is a collaborative investigator in the Mucosal HIV and Immunobiology Center (MHIC) at UAB. 
The central focus of the Elson laboratory is on the regulation of mucosal immune responses, particularly the mucosal immune response to the microbiota, which represent the largest mass of antigen encountered by the immune system. The cellular and molecular mechanisms that maintain mucosal immune homeostasis are being defined. When these mechanisms fail, pathogenic effector T cells are generated that result in colitis. Dr Elson and co-workers have cloned a set of immunodominant antigens of the microbiota that stimulate such pathogenic T cells and result in inflammatory bowel disease. Among these cloned antigens, previously unknown bacterial flagellins have emerged as a major cluster. Seroreactivity to these flagellins is found in multiple experimental models of colitis in mice and in half of patients with Crohn’s disease. These antigens drive a newly described CD4 T cell effector subset making IL-17 (Th17) which appears to be responsible for disease progression. A T cell receptor transgenic mouse reactive to the flagellins has been generated and is being used to study the innate and adaptive immune response to microbiota antigens. A second major effort is in the identification of T reg cells in the intestine that recognize microbial antigens and maintain homeostasis. The mechanisms whereby such cells are induced are being defined and the application of these cells to prevent or treat intestinal inflammation is being tested. 


Recent Publications
  1. Monoclonal anti-interleukin 23 reverses active colitis in a T cell-mediated model in mice.
    Elson CO, Cong Y, Weaver CT, Schoeb TR, McClanahan TK, Fick RB, Kastelein RA.
    Gastroenterology. 2007 Jun;132(7):2359-70
  2. Molecular approaches to the role of the microbiota in inflammatory bowel disease.
    Elson CO, Cong Y, Qi F, Hershberg RM, Targan SR. Ann N Y Acad Sci. 2006 Aug;1072:39-51.
  3. From cheese to pharma: a designer probiotic for IBD.
    Elson CO. Clin Gastroenterol Hepatol. 2006 Jul;4(7):836-7.
  4. Alterations of T lymphocytes in inflammatory bowel diseases.
    Elson CO, Cong Y, Weaver CT. Adv Exp Med Biol. 2006;579:133-48.
  5. Experimental models of inflammatory bowel disease reveal innate, adaptive, and regulatory mechanisms of host dialogue with the microbiota.
    Elson CO, Cong Y, McCracken VJ, Dimmitt RA, Lorenz RG, Weaver CT. Immunol Rev. 2005 Aug;206:260-76. Review.
  6. Lodes MJ, Cong Y, Elson CO, Mohamath R, Landers CJ, Targan SR, Fort M, Hershberg RM.  Bacterial flagellin is a dominant antigen in Crohn’s disease.  J Clin Invest 2004; 113:1296-1306.
  7. Cong Y, Feng T, Fujihashi K, Schoeb TR, and Elson CO.  Dominant, coordinated T regulatory cell-IgA response to the intestinal microbiota.  PNAS USA.  2009; 106:19256-61. PMID: 19889972
  8. Feng T, Wang L, Schoeb TR, Elson CO, Cong Y. Microbiota innate stimulation is a prerequisite for T cell spontaneous proliferation and induction of experimental colitis. J Exp Med. 2010; 6:1321-32. J Exp Med. 2010; 7:1569. PMID: 20498021
  9. Saleh M, Elson CO.  Experimental inflammatory bowel disease: insights into the host-micrbiota dialog. Immunity. 2011; 3:293-302.  PMID: 21435584
  10. Feng, T., Cong, Y., Alexander, K., & Elson, C. O. (2012). Regulation of Toll-like receptor 5 gene expression and function on mucosal dendritic cells. PloS One, 7(4), e35918. doi:10.1371/journal.pone.0035918 
  11. Feng, T., Qin, H., Wang, L., Benveniste, E. N., Elson, C. O., & Cong, Y. (2011). Th17 cells induce colitis and promote Th1 cell responses through IL-17 induction of innate IL-12 and IL-23 production. Journal of Immunology 186(11), 6313–6318. doi:10.4049/jimmunol.1001454
  12. Cao, A. T., Yao, S., Gong, B., Elson, C. O., & Cong, Y. (2012). Th17 Cells Upregulate Polymeric Ig Receptor and Intestinal IgA and Contribute to Intestinal Homeostasis. The Journal of Immunology. doi:10.4049/jimmunol.1200955
  13. Elson, C. O., & Cong, Y. (2012). Host-microbiota interactions in inflammatory bowel disease.  Gut Microbes, 3(4), 332–344.
  14. Hand, T. W., Santos, Dos, L. M., Bouladoux, N., Molloy, M. J., Pagán, A. J., Pepper, M., et al. (2012). Acute Gastrointestinal Infection Induces Long-Lived Microbiota-Specific T Cell Responses. Science (New York, NY). doi:10.1126/science.1220961 
  15. Maynard, C. L., Elson, C. O., Hatton, R. D., & Weaver, C. T. (2012). Reciprocal interactions of the intestinal microbiota and immune system. Nature, 489(7415), 231–241. doi:10.1038/nature11551
  16. Weaver, C. T., Elson, C. O., III, Fouser, L. A., & Kolls, J. K. (2012). The Th17 Pathway and Inflammatory Diseases of the Intestines, Lungs, and Skin. Annual Review of Pathology: Mechanisms of Disease, 8(1), 121116135809005. doi:10.1146/annurev-pathol-011110-130318