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Hansen's Disease Research

Edward J. Shannon

Dr. Edward J. Shannon image.

Senior Research Immunologist
Ph.D. 1974
University of Illinois
Champaign-Urbana, Illinois
eshann1@lsu.edu

Erythema nodosum leprosum (ENL) is an inflammatory complication that can occur in multibacillary HD patients. The treatment of choice is thalidomide. The sequence of events, which cause ENL as well as the mechanism(s) by which thalidomide and/or steroids arrest ENL have not been elucidated.

In clinical trials and sepsis studies in rodents, thalidomide is able to augment or to suppress the synthesis of inflammatory cytokines, especially TNF-alpha. Consequently, interpretation of the literature regarding thalidomide’s ability to regulate the “cytokine storm” in inflammatory conditions is confusing.

My research efforts are to determine thalidomide’s effect on three major cytokines, TNF-alpha, IL-6 and IL-8. These are involved in systemic inflammatory response syndromes. I am also interested in investigating a role for thalidomide in antibody synthesis and activation of complement. This is based on evidence that antibody and complement may be involved in the ENL reaction, and recent observations that thalidomide, in combination with dexamethasone, has a therapeutic effect on patients with multiple myeloma, a condition in which immunoglobulin synthesis continues unabated. In collaboration with investigators in the Research Branch and other institutions, we are studying the effect of thalidomide on various functions of schwann cells. This is based on reports that continuous use of thalidomide, especially in treating conditions other than ENL, can induce neuritis.

Representative Publications

Tadesse, A., Shannon, E.J. Effects of thalidomide on intracellular Mycbacterium leprae in normal and activated macrophages. Clinical and Diagnostic Laboratory Immunology 12(1): 30-134, 2005.

Tadesse,A., Abebe, M.,Bizuneh, E., M., A. Aseffa, Shannon, E.J. The effect of thalidomide on the expression of TNF mRNA and the synthesis of TNF in cells from leprosy patients with reversal reaction. Immunopharmacology and Immunotoxicology, 28:1-11, 2006.

E. J. Shannon, R. Noveck, F. Sandoval, B. Kamarth , M. Kearney.  Thalidomide suppressed IL-6 but not TNF-α in volunteers with experimental endotoxemia Translational Research150(5), 275-280, 2007.

E. J. Shannon, F. G. Sandoval. Thalidomide and thalidomide transformed by pH dependent hydrolysis or by liver enzyme treatment does not impede the proliferation of endothelial cells, Immunopharmacology and Immunotoxicology. 30:307-316, 2008.  

E. J. Shannon, R. Noveck F. Sandoval, B. Kamarth  Thalidomide suppressed IL-1 beta while enhancing TNF-alpha and IL-10, when cells in whole blood were stimulated with lipopolysaccharide, Immunopharmacology and Immunotoxicology 30:447-457,2008. 

R. Lahiri, F. Sandoval, J. Krahenbuhl, E. J. Shannon.
Activation of Complement by Mycobacterium leprae requires disruption of the bacilli. Lepr Rev 79 (3): 311-314, 2008.
                       
Anna Israyelyan, E. J. Shannon, Abolghasem Baghian, Michael T. Kearney, Konstantin G. Kousoulas Thalidomide Suppressed the Growth of 4T1 cells into Solid Tumors in Balb/c Mice in a Combination Therapy with the Oncolytic Fusogenic HSV-1 OncdSyn, Cancer Chemother Pharmacol. 64(6):1201-10, 2009.

E. J. Shannon, Sandoval F Thalidomide inhibited the synthesis of IgM and IgG whereas Thalidomide+Dexamethasone and Dexamethasone alone acted as co-stimulants with pokeweed and enhanced their synthesis. Int. Immunopharmacol.Apr;10(4):487-92, 2010.

Ladizinski B, Sanchez M, E. J. Shannon, W. Levis. Thalidomide and analogs: Potential for immunoduation and inflammatory and Neoplastic Dermatologic Disorders, Journal of Drugs in Dermatology (review article) 9(7) 1-14, 2010.