Physiological caffeine concentrations do not affect enteric neural crest cell migration in a mouse model

Abstract

The defect in enteric neural crest cell (ENCCs) migration that causes Hirschsprung disease (HD) in newborns is linked to genetic and likely also environmental factors. Among these, maternal coffee consumption has been associated with increased HD risk, yet the role of caffeine on ENCC migration has remained unexplored. Here, we show that although mouse ENCCs express caffeine-sensitive ADORA2A receptors, physiological doses of caffeine do not perturb endogenous ENCC calcium activity. We find that caffeine can modulate ENCC outgrowth in a 2D culture model but that it does not affect migration in a 3D collagen gel and in the ex-vivo embryonic gut. We conclude that physiological doses of caffeine do not hamper ENCC migration in the ex-vivo embryonic mouse intestine, thereby discarding a potential direct environmental mechanism of caffeine in HD.

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BibTeX

@misc{romito2026physiological,
  title = {{Physiological caffeine concentrations do not affect enteric neural crest cell migration in a mouse model}},
  author = {O. Romito and J. Peres and M. Dicu and E. Lelong and I. Le Parco and N. Bondurand and N. R. Chevalier},
  howpublished = {bioRxiv},
  year = {2026},
  month = nov,
  doi = {10.64898/2026.11.03.763904},
  url = {https://www.biorxiv.org/content/10.64898/2026.11.03.763904v1},
  note = {CC BY-NC-ND},
}

RIS

TY  - UNPB
TI  - Physiological caffeine concentrations do not affect enteric neural crest cell migration in a mouse model
AU  - O. Romito
AU  - J. Peres
AU  - M. Dicu
AU  - E. Lelong
AU  - I. Le Parco
AU  - N. Bondurand
AU  - N. R. Chevalier
PY  - 2026
DA  - 2026/11/03
PB  - bioRxiv
DO  - 10.64898/2026.11.03.763904
UR  - https://www.biorxiv.org/content/10.64898/2026.11.03.763904v1
AB  - The defect in enteric neural crest cell (ENCCs) migration that causes Hirschsprung disease (HD) in newborns is linked to genetic and likely also environmental factors. Among these, maternal coffee consumption has been associated with increased HD risk, yet the role of caffeine on ENCC migration has remained unexplored. Here, we show that although mouse ENCCs express caffeine-sensitive ADORA2A receptors, physiological doses of caffeine do not perturb endogenous ENCC calcium activity. We find that caffeine can modulate ENCC outgrowth in a 2D culture model but that it does not affect migration in a 3D collagen gel and in the ex-vivo embryonic gut. We conclude that physiological doses of caffeine do not hamper ENCC migration in the ex-vivo embryonic mouse intestine, thereby discarding a potential direct environmental mechanism of caffeine in HD.
ER  -

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