Emilie Viennois

Website: https://cri1149.fr/en/equipes/hugot/
ORCID: 0000-0002-3104-620X
Twitter: @EViennois

Increasing evidence has implicated a disruption of host immune-microbial interaction and luminal microbial dysbiosis – term referring to an alteration of the intestinal microbiota – in the pathogenesis of IBD and other chronic inflammatory disorders. Our research focuses on considering the intestinal interface between the outer and the inner parts of the intestine, seeking to explain how this interface operates to mediate host-microbiota interactions impacting the physiopathology of chronic inflammatory diseases. Notwithstanding our interest for IBD, we also explore other chronic inflammatory diseases related to an altered host-microbiota dialogue, such as arthritis. Both conditions are used and seen as diseases model of intestinal and extra-intestinal inflammation. Our central objective aims to understanding how the gut interface can be determining in the initiation and development of dysbiosis-associated diseases appears crucial.

Dysbiosis, early in life, has now been appreciated for its determining impact on intestinal health later in life. Several evidences made in both humans and mice indicate that individuals having a reduced contact with lives microbes, develop a pathological imprinting to IBD and to other chronic disorders such as rheumatoid arthritis later in life. In contrast, higher bacterial diversity in early life prevents illness development in adulthood. Therefore, our project focuses on both early events and those at the time of the disease.

Our fundamental question, fueled by clinical observations, is addressed according to three axes:
1) Explore how the outside world (environment, microbiota, diet) does impact the interface (OUTER). In an ongoing prospective exposed/non-exposed study, « MIKINAUTEs », we seek to understand how exogenous factors (food and exposome) can influence relapse and/or remission in IBD.

2) Understanding the interface itself (INTERFACE) with a special focus on intestinal miRNA and their role in host-microbiota interaction and more generally intestinal homeostasis.

3) Examine how the deregulation of the interface does impact distant organs potentially leading to extra-intestinal pathologies (INNER) such as arthritis. This axe seeks to determine how alterations of the intestinal barrier function and bacterial translocation can promote IBD, and similarly arthritis, and autoimmunity in genetically predisposed hosts.

Top 5 publications

1. Casado-Bedmar M, Viennois E. microRNA and gut microbiota: Tiny but mighty – Novel insights of their crosstalk in inflammatory bowel disease pathogenesis and therapeutics. J Crohns Colitis. 2022 Jul 14;16(6):992-1005.
2. Naimi S, Viennois E, Gewirtz AT, Chassaing B. Direct impact of commonly used dietary emulsifiers on human gut microbiota. 2021 Mar 22;9(1):66.
3. Viennois E, Pujada A, Sung J, Yang C, Gewirtz AT, Chassaing B, Merlin D. Impact of PepT1 deletion on microbiota composition and colitis requires multiple generations. NPJ Biofilms Microbiomes. 2020 Jul 21;6(1):27.
4. Viennois E, Bretin A, Dubé PE, Maue AC, Dauriat CJG, Barnich N, Gewirtz AT, Chassaing B. Dietary Emulsifiers Directly Impact Adherent-Invasive E. coli Gene Expression to Drive Chronic Intestinal Inflammation. Cell Rep 2020 Oct 6;33(1):108229.
5. Viennois E, Chassaing B, Tahsin A, Pujada A, Wang L, Gewirtz A.T., Merlin D. Host-derived fecal microRNAs can indicate gut microbiota healthiness and ability to induce inflammation. Theranostics 2019; 9(15): 4542-4557.

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