IL-22 from enteroendocrine cells promotes early-life gut motility in zebrafish through the microbiota
Summary
The gut microbiota, immune system, and enteric nervous system interact to regulate adult gut physiology. However, the mechanisms establishing gut physiology during development remain unknown. We report that in developing zebrafish, enteroendocrine cells produced interleukin-22 (IL-22) in response to microbial signals before lymphocytes populated the gut. In larvae, IL-22 shaped the gut microbiota, increasing Lactobacillaceae abundance and ghrelin expression to promote gut motility. Impaire
Content
# IL-22 from enteroendocrine cells promotes early-life gut motility in zebrafish through the microbiota
*Published: 2026 Apr 2*
The gut microbiota, immune system, and enteric nervous system interact to
regulate adult gut physiology. However, the mechanisms establishing gut
physiology during development remain unknown. We report that in developing
zebrafish, enteroendocrine cells produced interleukin-22 (IL-22) in response to
microbial signals before lymphocytes populated the gut. In larvae, IL-22 shaped
the gut microbiota, increasing Lactobacillaceae abundance and ghrelin expression
to promote gut motility. Impaired motility and ghrelin expression were restored
in il22-/- zebrafish by transfer of microbiota from wild-type zebrafish or by
introducing only Lactobacillus plantarum. IL-22-deficient mice also had impaired
gut motility and reduced ghrelin expression in early life, indicating a
conserved function. Thus, before immune system maturation, enteroendocrine cells
regulate early-life gut function by controlling the microbiota through IL-22.
DOI: 10.1126/science.adr1707