The intestinal microbiota fascinates scientists as much as it intrigues the general public. This immense community of bacteria, viruses and fungi installed in our digestive system plays a central role in digestion, immunity and even certain brain functions. Until now, researchers knew that the immune system helps maintain the balance between the gut and this microbiota. But a question remained: how is this relationship organized in newborns, when their immune system is still immature?
In a study published on April 2, 2026 in the journal
Sciencea team of researchers from the Institut Curie, Inserm and the CNRS provides an unexpected answer. Their work shows that certain intestinal cells take over very early in life to communicate with the microbiota and organize good intestinal functioning.
Intestinal cells capable of acting like the immune system
To carry out their research, the scientists relied on zebrafish, a model widely used in developmental biology. From their first day of life, these animals are already exposed to the microorganisms present in their environment, even though their immune defenses are not yet fully developed.
Researchers then discovered that specialized cells in the intestine, called enteroendocrine cells, produce a key immune molecule: interleukin-22, or IL-22. Until now, this substance was considered to be produced only by certain immune cells, lymphocytes.
Even more surprising, this production is directly stimulated by the microbiota itself. Intestinal microorganisms trigger this mechanism thanks to a metabolite derived from tryptophan, an amino acid present in particular in food. In return, IL-22 acts on the intestine by activating antimicrobial genes capable of shaping the composition of the microbiota.
The researchers thus describe a real circle of interactions: the microbiota influences the intestine, which then acts on the microbiota to maintain a balance essential to digestive development.
A direct impact on intestinal transit
The study also reveals that this early dialogue between intestine and microbiota is not limited to immunity. It also plays a major role in intestinal motility, in other words the ability of the intestine to move food through the digestive tract.
In young animals deprived of IL-22, scientists observed a slowdown in transit as well as a drop in levels of ghrelin, a hormone best known for stimulating appetite. This hormone also seems capable of partly compensating for the effects of the lack of IL-22 on intestinal functioning.
These results suggest that the digestive disorders observed in certain infants could be linked, at least in part, to very early disruptions in exchanges between microbiota and the intestine.
A promising avenue for future treatments
Beyond this fundamental discovery, the researchers believe that these mechanisms could become new therapeutic targets. Ultimately, they could make it possible to better treat certain inflammatory disorders or intestinal motility problems occurring early in life.
This work also changes the way we look at enteroendocrine cells. Long considered as simple hormonal cells, they now appear as true multitasking cells, capable of intervening in immunity, intestinal development and perhaps even tissue repair.
Scientists now wish to explore their role in the regeneration of the intestine after severe injury. A new step which could reveal other still unsuspected functions of these discreet but essential cells.