Alain Stintzi

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.

Two circular graphs composed of a variety of ribbons, displaying the expression of genes in iron activated versus iron repressed conditions.

Individual genes that were found to be differentially expressed between iron limiting and iron replete conditions were sorted by COG category and plotted based on their degree of differential expression.

Research Program

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.

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