• Steiner, Ted


    Investigator, BC Children's Hospital
    Professor, Division of Infectious Diseases, Department of Medicine, University of British Columbia
    Associate Head, UBC Division of Infectious Diseases

    Degrees / Designations


    Primary Area of Research
    Childhood Diseases
    Secondary Area(s) of Research
    604-875-2000 ext. 4910
    Lab Phone
    Mailing Address

    BC Children's Hospital Research Institute
    Room A4-146
    950 West 28th Avenue
    Vancouver, BC V5Z 4H4

    Affiliate Websites
    Research Areas
    • Intestinal Immunology
    • Gastrointestinal Infections
    • C. difficile Infection
    • Inflammatory Bowel Disease
    • Intestinal Epithelial Biology

    The human gut is a very complex system that affects many areas of health. For the gut to work normally, there must be coordination between the immune system, nervous system, and multiple different cell types that line the gut and help it to process and absorb food while fighting infections. The gut also carries a huge number of microbes that play important roles in maintaining its functions. My work focuses on the way that the intestinal immune system functions to fight infections while maintaining normal relationships with the "good" bacteria that normally live in the gut.

    Current Projects

    My current research program targets two very important intestinal diseases: C. difficile infection and inflammatory bowel disease. C. difficile is the leading cause of hospital-acquired infections in Canada, and can lead to debilitating or even fatal diarrhea. I am exploring the role of the immune system in protecting against C. difficile by studying specific types of immune responses in people with their first episode of infection and comparing them to people with recurrent infections. I also have several clinical projects examining the benefit of fecal microbial transplantation (FMT), also known as "stool transplant", to control these recurrent infections.

    My second main project is to develop a new treatment for inflammatory bowel disease (IBD; ulcerative colitis and Crohn's disease) based on the realization that people with these diseases develop abnormal immune responses to normal gut bacteria. It is believed that these responses "trick" the gut into thinking there is a bad infection, so it mobilizes its "army" of white blood cells into the gut, leading to unwanted inflammation that damages the gut. We are working to take advantage of these abnormal responses by making "super-suppressor" cells that reduce inflammation when they sense a major bacterial protein, flagellin, which is present in large amounts in the gut. We are also examining the types of immune responses that people with IBD make against flagellin to better understand how they cause damage.

    Selected Publications

    Shane AL, Mody RK, Crump JA, Tarr PI, Steiner TS, Kotloff K, Langley JM, Wanke C, Warren CA, Cheng AC, Cantey J, Pickering LK. 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea. Clin Infect Dis. 2017 Oct 19. [Epub ahead of print].

    Manges AR, Steiner TS, Wright AJ. Fecal microbiota transplantation for the intestinal decolonization of extensively antimicrobial-resistant opportunistic pathogens: a review. Infect Dis (Lond). 2016 Aug;48(8):587-92. Epub 2016 May 19. Review.

    Steiner TS. (2016). New Insights into Shiga Toxigenic Escherichia coli Pathogenesis: When Less Is More. J. Infect. Dis. 213(8): 1214-5.

    Christine H. Lee, M.D., Theodore Steiner, M.D., Elaine O. Petrof, M.D., Marek Smieja, M.D., Ph.D, Diane Roscoe, M.D., Anouf Nematallah, M.D., J. Scott Weese, D.V.M., Stephen Collins, M.B.B.S., Paul Moayyedi, M.B., Mark Crowther, M.D., Mark J. Ropeleski, M.D, David Higgins, M.B., Yingfu Li, Ph.D., and Peter T. Kim, Ph.D. A Randomized Trial of Fresh vs. Frozen Fecal Transplantation for C. difficile Infection.  JAMA 2016 Jan 12;315(2):142-9.

    Yu Yao, Jens Vent-Schmidt, Matthew D. McGeough, May Wong, Hal M. Hoffman, Theodore S. Steiner*, Megan K. Levings*. Tr1 cells, but not Foxp3+ Tregs, suppress NLRP3 inflammasome activation via an IL-10 dependent mechanism. J Immunol. 2015 Jul 15;195(2):488-97.

    Yeung SS, Yeung JK, Lau TT, Forreste LA, Steiner TS, Bowie WR, Bryce EA. Evaluation of a Clostridium difficile infection management policy with clinical pharmacy and medical microbiology involvement at a major Canadian teaching hospital. J Clin Pharm Ther. 2015 Nov 7.

    Steiner TS. The Worst of Both Worlds: Examining the Hypervirulence of the Shigatoxigenic/Enteroaggregative Escherichia coli O104:H4. J Infect Dis. 2014 Jul 18.

    Sheridan J, Mack DR, Amre DK, Israel DM, Cherkasov A, Li H, Grimard G, Steiner TS. A non-synonymous coding variant (L616F) in the TLR5 gene is potentially associated with Crohn's disease and influences responses to bacterial flagellin. PLoS One. 2013 Apr 11;8(4):e61326.

    Himmel ME, MacDonald KG, Garcia RV, Steiner TS, Levings MK. Helios+ and Helios- cells coexist within the natural FOXP3+ T regulatory cell subset in humans. J Immunol. 2013 Mar 1;190(5):2001-8.

    Yao Y, Levings MK, Steiner TS. ATP conditions intestinal epithelial cells to an inflammatory state that promotes components of DC maturation. Eur J Immunol. 2012 Dec;42(12):3310-21.


    Canadian Institutes of Health Research (CIHR) Project Grant 2017-2021

    Crohn's & Colitis Foundation of Canada (CCFC) Grants in Aid of Research 2016-2019

    Canadian Institutes of Health Research (CIHR) Operating Grant 2017-2019

    BC Transplant Foundation BCTRF Venture Grants 2016-2018

    Honours & Awards
    Research Group Members