Professor Tor C. Savidge

Tor C. Savidge, Ph.D. is Associate Professor, Division of Gastroenterology and Hepatology, University of Texas Medical Branch.
 
Tor earned his Ph.D. degree in Molecular Cell Biology from the University of Cambridge, UK. He then did his postdoctoral training in the UK before assuming a faculty position at Harvard Medical School and also served as a Director of the NIH-Clinical Nutrition Research Center at Harvard for 5 years prior to joining UTMB. He has been funded by the NIH and numerous Research Foundations for his gastrointestinal work and is a recipient of several awards: a Senior Investigator Award from the Crohn’s and Colitis Foundation of America, Broad Medical Research Foundation Award, and a John S. Dunn Foundation Collaborative Research Award. He is a member of several international editorial boards and will soon be the Editor-in-Chief for the Open Gastroenterology Journal until 2013.
 
Tor also serves on the Editorial Boards of Frontiers in Enteric Neuroscience, World Gastroenterology Journal, ISRN Gastroenterology, World Journal of Gastrointestinal Pharmacology and Therapeutics (WJGPT), and World Journal of Translational Medicine.
 
He also serves as an invited faculty member of Faculty-of-1000 Medicine, a prestigious post-publication peer review publication that advises the general scientific and medical community on important new clinical practices and scientific advances. Since 1999 he has served on National Institute of Health Study Sections, Review sections for the American Gastroenterology Association, the Clinical Nutrition Research Center at Harvard, the Broad Foundation and the Research Advisory Committee at UTMB. He has published over 60 articles, has coedited one book on Microbial Imaging and recently edited a Special Highlights Topic on Clostridium difficile infection for the World Gastroenterology Journal where he currently serves as an Editorial Board Member.
 
Tor has proposed the hypothesis that a failure in enteric glial cell function may contribute towards inflammation in Crohn’s disease patients, a feature currently regarded as a likely primary cause for the recurrent pathology. He has identified a new signaling molecule produced by enteric glial cells known as S-nitrosoglutathione (GSNO) that drastically reduces intestinal permeability and inflammation in colonic biopsies from Crohn’s disease patients. This molecule is normally produced in the human colon, but in Crohn’s disease patients levels are significantly diminished for unknown reasons.
 
He is currently funded by the NIH to investigate whether aberrant GSNO production translates into intestinal inflammation. His studies indicate that GSNO has a significant therapeutic potential in inflammatory bowel disease and this also forms the basis of a patent in which he is the Principal Investigator. As part of his NIH grant and Broad Foundation Award, he is now actively identifying the mechanism for the protective GSNO effects on intestinal inflammation.
 
Tor is also the recipient of an NIH-ITS grant and an Award from the John S. Dunn Gulf Coast Consortium for Chemical Genomics Robert A. Welch Collaborative Grant Program to use his expertise of GSNO chemistry and computational methods to develop novel therapeutic compounds for intestinal inflammation. In addition to Crohn’s disease, these grants focus on Clostridium difficile-induced colitis, which is the leading cause of antibiotic-associated diarrhea and colonic inflammation in the United States.
 
As Principal Investigator of an NIH-funded multidisciplinary team at UTMB, he is initiating a clinical trial to assess whether disease amelioration is evident in patients with Clostridium difficile patients using methods that Tor has pioneered in his laboratory. The impact of developing effective oral small molecule therapy for such an important infectious pathogen is that this would provide an inexpensive and novel treatment option for a global epidemic that threatens to become one of the major public health concerns of the 21st century.
 
His papers include Apoptosis of Human Intestinal Epithelial Cells after Bacterial Invasion, Role of Intestinal Epithelial Cells in the Host Secretory Response to Infection by Invasive Bacteria: Bacterial Entry Induces Epithelial Prostaglandin H Synthase-2 Expression and Prostaglandin E₂ and F_2α Production, Enterocolitis induced by autoimmune targeting of enteric glial cells: A possible mechanism in Crohn’s disease?, Developmentally regulated IκB expression in intestinal epithelium and susceptibility to flagellin-induced inflammation, Characterization of Candidate Live Oral Salmonella typhi Vaccine Strains Harboring Defined Mutations in aroA, aroC, and htrA, and Clostridium difficile Toxin A Regulates Inducible Cyclooxygenase-2 and Prostaglandin E₂ Synthesis in Colonocytes via Reactive Oxygen Species and Activation of p38 MAPK.