CV Science

David RIBET PhD Microbiology, Research Associate, INSERM

Course and current status

Since 2017 : Research Associate (CRCN INSERM) in the "Nutrition, Inflammation and Microbiota-Gut-Brain Axis" Lab (INSERM UMR 1073; Pr. Moïse COËFFIER), Rouen University, Rouen, France.

2011-2017 : Research Associate (CRCN INSERM) in the "Bacteria-Cell Interactions" Lab (INSERM U604; Pr. Pascale COSSART), Institut Pasteur, Paris, France.

2007-2011 : Post-Doctoral fellow in the "Bacteria-Cell Interactions" Lab (INSERM U604; Pr. Pascale COSSART), Institut Pasteur, Paris, France.

Diplomas :

2016 : Habilitation à Diriger des Recherches (HDR)

2009 : Training in Cellular Microbiology (Diplôme Universitaire), University of Lille, France.

2007 : Ph.D. in Microbiology / Virology, Paris Diderot University, France.

2003 : Master's degree in Microbiology / Virology, Paris Diderot University, France.

2002 : Agrégation de Sciences de la Vie et de la Terre.

2001 : Bachelor's degree in Biochemistry, Paris Diderot University, France.

1999-2003 : Training in Ecole Normale Supérieure de Cachan, France.

Scientific summary

Gut microbiota, SUMOylation and intestinal pathophysiology

    The gut microbiota produces a wide variety of metabolites, which modulate intestinal cell activities and participate to human physiology. The effect of gut bacteria on SUMOylation, an essential ubiquitin-like modification in intestinal physiology, has mainly been investigated in the case of bacterial pathogens. These pathogens inhibit intestinal SUMOylation to promote infection. We have recently demonstrated that gut commensal bacteria, in contrast to pathogens, increase intestinal protein SUMOylation via the production of specific metabolites. This “hyperSUMOylation” results in the dampening of inflammatory responses of enterocytes in vitro. These metabolites thus constitute interesting drug candidates to dampen intestinal inflammation in vivo.

    My current research projects aim to (1) Identify gut bacteria/metabolites able to modulate intestinal SUMOylation, (2) Determine how modulation of SUMOylation triggered by gut bacteria modifies intestinal cell physiology and (3) Determine whether gut bacteria/metabolites modulating SUMOylation may dampen inflammation in pre-cinical models of inflammatory bowel diseases (IBD).

    These projects will provide new insights into previously uncharacterized interactions between intestinal cells and gut bacteria. They may also identify potential new therapeutics for the treatment of prevalent human inflammatory diseases.