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

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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Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2026-11-04
DOI
https://doi.org/10.64898/2026.11.03.763904
Primary Topic
Congenital gastrointestinal and neural anomalies
Type
preprint
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preprint

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

Olivier Romito, Monica Dicu, Nadège Bondurand, Nicolas R. Chevalier et al.
bioRxiv (Cold Spring Harbor Laboratory)
Congenital gastrointestinal and neural anomalies
preprint

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

Olivier Romito, Monica Dicu, Nadège Bondurand, Nicolas R. Chevalier, Isabelle Le Parco, Justine Peres, Emeline Lelong
preprint en

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.

bioRxiv (Cold Spring Harbor Laboratory)
Université Paris Cité (FR), Institut Jacques Monod (FR), Laboratoire Matière et Systèmes Complexes (FR), Institut des Maladies Génétiques Imagine (FR)
Congenital gastrointestinal and neural anomalies
DOIOpen Access PDFOpenAlex
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Physiological caffeine concentrations do not affect enteric neural crest cell migration in a mouse model — Olivier Romito, Monica Dicu, et al. · bioRxiv (Cold Spring Harbor Laboratory) (2026) | TGRS Research Map | TGRS