The prenatal period is a delicate time during which intrauterine ex-posure to environmental factors may modulate the course of devel-opment of the intestinal barrier function and the sensory system,thereby increasing the risk of developing functional disorders. Wehypothesized that prenatal stress in mice would predispose adult off-spring to visceral hypersensitivity and intestinal homeostasis failure.Prenatal stress was induced by using a restriction stress with brightlight during 30 minutes, three times a day, in female mice betweenday 13 and 18 of gestation. In 8 weeks old offspring, visceral sensi-tivity to colorectal distention and intestinal paracellular permeabilitywere assessed in male and female. Mucus, tight junction proteins,anti-microbial peptides, chemokines and cytokines were moni-tored by qPCR and intestinal bioactive lipids by mass spectrometry.MiSeq-based microbial taxonomic analysis was used to determinefaecal microbiota composition. Prenatal stress induced visceral hy-persensitivity and increased paracellular permeability in the majorityof male and female offspring. Only in male, we quantified a decreasein 5-lipoxygenase activity and Tnfα expression and an increase inTtf3 and Ifnγ expression. Prenatal stress induced in male and femaleadult offspring a dysbiosis characterized in male by a decrease inintestinal microbiota diversity, an increase in Akkermansia and a de-crease in Desulfovibrio and in female by an increase in Akkermansiaand a decrease in Lactobacillus animalis. Interestingly, the abundancein Lactobacillus animalis was inversely correlated with visceral hyper-sensitivity. Prenatal stress is sufficient to induce microbiota dysbio-sis, visceral hypersensitivity and increase paracellular permeabilityin adulthood. Thus, prenatal stress could represent a priming eventfor the development of functional disorders in adulthood.
Petitfils, C., & et al. (2020). Impact of prenatal stress on visceral sensitivity and intestinal homeostasis in adulthood. Neurogastroenterology and Motility, 32(S1), e13817. https://doi.org/10.1111/nmo.13817 (Original work published 2020)