Abstract of talk

The gastro-intestinal tract is heavily colonised by a complex community of microorganisms called the intestinal microbiota, which play numerous roles in both health and diseases. In his presentation, Benoit Chassaing will present his work related to the detrimental impact of various emulsifiers on the intestinal microbiota. Research carried out by his team has indeed demonstrated that various emulsifiers can directly alter the intestinal microbiota, both compositionally and functionally, in a way that can promote numerous chronic inflammatory diseases, metabolic deregulation and susceptibility to colon cancer. 
Mechanistically, dietary emulsifiers directly target the intestinal microbiota, with the observation that germfree models are protected against emulsifier-detrimental impacts, while faecal microbiota transplantation is sufficient to transfer chronic intestinal inflammation and metabolic deregulation. Moreover, dietary emulsifiers directly target select members of the intestinal microbiota to promote their pathogenic potential.
A recent clinical trial highlighted the potential detrimental impact of emulsifiers on intestinal and human health, with the observation that short-term exposure of healthy individuals to Carboxymethylcellulose – E466 – is sufficient to induce microbiota alterations, faecal metabolome depletion and microbiota encroachment within the normally sterile mucus layer.
We will also discuss the impact of various other food additives, with the important observation that not all the commonly used dietary emulsifiers detrimentally impact the intestinal microbiota. Moreover, we will discuss the importance of inter-individual variations in microbiota composition in driving the response/susceptibility to dietary emulsifiers, with the observation that while some microbiota are fully protected against the detrimental impact of emulsifiers, some other microbiota, hosting select microbiota members, are highly susceptible to emulsifier-induced disturbance and following chronic intestinal inflammation, metabolic deregulation.