Vice-Dean, Office of Graduate and Postdoctoral Studies
Work: 613) 562-5800 ext. 8216
Humans coexist with large and complex microbial communities that colonize various bodily sites, such as the skin, the vagina and the gastrointestinal tract. Currently, we know very little about how these microbial communities interact, influence or communicate with the host. What is their role in preserving health or contributing to disease? What are the microbial biological processes that interact with the host and affect human health? How do microbial pathogens compete or cooperate with the host’s microbial communities to cause disease? Our research seeks to address these key questions.
The Stintzi lab accepts students from graduate programs in Biochemistry and Microbiology and Immunology.
The gut mucosa is the body’s first barrier against microbial invaders. The major mucosa defense mechanisms consist of the resident gut microbiota, the mucus layer, and the immune system. A key component of the immune system is known as “nutritional immunity” where the host sequesters vital nutrients—such as the transition metals iron, manganese and zinc—from invading pathogens.
The mechanisms used by enteric pathogens to subvert the host’s mucosa defenses remain poorly understood. Understanding the functional dialogue between the host, the resident microbiota and the invading pathogen is paramount in elucidating these mechanisms. One objective of our research is to understand how enteric pathogens such as Campylobacter jejuni acquire essential nutrients, adapt to the harsh conditions of the intestine and interact with the host’s microbiota to cause disease.
Alterations in the composition of the gut microbiota have also been associated with numerous diseases, including irritable bowel syndrome, inflammatory bowel disease (IBD), insulin resistance, cardiovascular disease and obesity. However, we don’t know whether alterations in the gut microbiota directly cause these diseases, are important in the chronicity of diseases or whether the altered compositions are simply consequences of diseases. The incidence of chronic non-genetic diseases has increased drastically over the past 50 years, implicating environmental factors. While the gut microbiome might help explain this alarming observation, we remain surprisingly ignorant of its specific role in disease.
The main objectives of our interdisciplinary research are to characterize the biological processes involved in disease pathogenesis (with a special emphasis on pediatric inflammatory bowel disease) at the microbiota-host interface and to exploit this information to manipulate the gut microbiota as a potential therapeutic treatment.
Martin Stahl and Alain Stintzi. 2011. Identification of essential genes in C. jejuni genome highlights hyper-variable plasticity regions. Functional and Integrative Genomics. Feb. 23. 11(2); 241-57.
Martin Stahl, Lorna Friis, Harlad Nothaft, Xin Liu, Jianjun Li, Christine Szymanski, and Alain Stintzi. 2011. L-fucose provides Campylobacter jejuni with a competitive advantage. Proc. Natl. Acad. Sci. USA. 108(17): 7194-7199.
Peter J. Turnbaugh and Alain Stintzi. 2011. Human health and disease in a microbial world. Front Microbiol. 2011;2:190. Epub 2011 Sep 16.
Flint A, Sun YQ, Stintzi A. 2012. Cj1386 is an ankyrin-containing protein involved in heme trafficking to catalase in Campylobacter jejuni. J Bacteriol. Jan; 194(2):334-45.
Martin Stahl, James Butcher and Alain Stintzi. 2012. Nutrition acquisition and metabolism by Campylobacter jejuni. Front. In Frontiers in Cellular and Infection Microbiology. Vol 2, article 5, p 1-10.
James Butcher, Sabina Sarvan, Joseph Brunzelle, Jean-Francois Couture and Alain Stintzi. 2012. Insights into the mechanism of Fur regulation in Campylobacter jejuni : a structural and genome-wide analysis. Proc Natl Acad Sci U S A. 2012 Jun 19;109(25):10047-52.
Arthur, JC, Perez-Chanona EP, Muhkbauer, M., Tomkovich, S., Uronis, JM, Fan, TJ, Abujamel, T., Dogan, B., Campbell, B.J., Rogers A.B., Rhodes, J.M., Simpson, K.W., Stintzi, A., Hansen, J.J., Keku, T.O., Fodor, A.A., and C. Jobin. 2012. Intestinal inflammation targets cancer-inducing activity of the microbiota. Science. 2012 Oct 5;338(6103):120-3
Merrell, DS and A. Stintzi. 2012. Research advances in the study of Campylobacter, Helicobacter and related organisms. Front Cell Infect Microbiol. 2012; 2:159.
Dufour V, Li J, Flint A, Rosenfeld E, Rivoal K, Georgeault S, Alazzam B, Ermel G, Stintzi A, Bonnaure-Mallet M, Baysse C. Inactivation of the LysR regulator Cj1000 of Campylobacter jejuni affects host colonisation and respiration. Microbiology. 2013 Apr 4.
Naikare H, Butcher J, Flint A, Xu J, Ramond K, and A. Stintzi. Campylobacter jejuni ferric-enterobactin receptor CfrA is TonB3 dependent and mediates iron acquisition from structurally different catechol siderophores. Metallomics, 2013 Aug;5(8):988-96.
Dufour, V., Stahl, M., Rosenfeld, E., Stintzi, A., and C. Baysse. Insights into the mode of action of benzylisothiocyanate on Campylobacter jejuni. 2013. Applied and Environmental Microbiology; Nov;79(22):6958-68.
Abujamel, T., Cadnum, J.L., Jury, L.A., Kundrapu, S., Jump, R.S., Stintzi, A. (co-corresponding author) and Donskey C. Defining the Vulnerable Period for Re-Establishment of Clostridium difficile Colonization After Treatment of C. difficile Infection with Oral Vancomycin or Metronidazole. 2013. PLoS One. 2013 Oct 2;8(10):e76269.
Butcher J and A. Stintzi. The transcriptional landscape of Campylobacter jejuni under iron replete and iron limited growth conditions. PLoS One. 2013 Nov 1;8(11):e79475