Speaker
Description
The mammalian gastrointestinal tract is a complex ecosystem that harbors trillions of microorganisms known as the gut microbiota. As microbes-host interactions are important to maintain host homeostasis, alterations in the microbial composition that lead to functional impairments can have detrimental consequences for the host (dysbiosis). In this context, diet represents one of the main environmental microbiota-disturbing causes that can affect the host’s status by mechanisms that remain to be determined. To establish a gnotobiotic model in which diet-induced dysbiosis can be mechanistically studied, we chose a murine gut-derived synthetic community, Oligo-Mouse-Microbiota-12 (OMM12), as a baseline to reduce the inherent complexity of the mammalian gut microbiota. OMM12-colonized mice, germ-free mice, and mice bearing conventional microbiota were exposed to a standard diet, as control, or a diet rich in simple sugars and saturated fats. The responses to these diets, at the microbiota and host levels, were evaluated. In this talk, I will present the comparison in the response of the different mice models to these nutritional inputs, and I will discuss the strategies we are implementing to refine a minimal synthetic community able to recapitulate the complex functional repertoire found in the native ecosystem.
