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Updated: Jun 23, 2026
A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Neonatal maternal deprivation triggers long term alterations in colonic epithelial barrier and mucosal immunity in
F Barreau1, L Ferrier, J Fioramonti
1Neurogastroenterology and Nutrition Unit, Institut National de la Recherche Agronomique, Toulouse, France.
Insights
Early life stress, like maternal deprivation, permanently damages the gut barrier in rats. This leads to increased inflammation and a heightened immune response to colitis triggers later in life.
Area of Science:
- Neurogastroenterology
- Immunology
- Developmental Biology
Background:
- Early life stress, such as maternal deprivation, can alter adult immune and gastrointestinal functions.
- Investigating the long-term effects of maternal deprivation on the colonic epithelial barrier is crucial.
Purpose of the Study:
- To determine if maternal deprivation impacts the colonic epithelial barrier in adult rats.
- To assess the effect of maternal deprivation on the development of experimental colitis.
Main Methods:
- Male Wistar rat pups underwent maternal deprivation or were undisturbed.
- Assessed colonic permeability, bacterial translocation, myeloperoxidase (MPO) activity, mast cell density, and cytokine mRNA expression.
- Induced colitis using 2,4,6-trinitrobenzenesulphonic acid (TNBS) to evaluate inflammatory response.
Main Results:
- Maternal deprivation increased colonic permeability and bacterial translocation.
- Elevated MPO activity, mast cell density, and pro-inflammatory cytokine mRNA were observed.
- Deprived rats showed exacerbated inflammatory responses and colonic damage when induced with TNBS colitis.
Conclusions:
- Maternal deprivation causes lasting changes to the colonic epithelial barrier.
- Early psychological factors influence the colonic mucosal barrier function in later life.
- These alterations result in an exaggerated immune response to external stimuli, predisposing to colitis.
Background:
Stressful events in the early period of life (for example, maternal deprivation) have been shown to modify adult immune and gastrointestinal tract functions. The present study aimed to establish whether maternal deprivation affects colonic epithelial barrier and the development of an experimental colitis in adult rats.
Methods:
Male Wistar rat pups were separated during postnatal days 2-14 or left undisturbed with their dam. At 12 weeks of age, we assessed colonic paracellular permeability, bacterial translocation, myeloperoxidase (MPO) activity, mucosal mast cell density, cytokine (interleukin (IL)-1 beta, IL-2, IL-4, IL-10, and interferon gamma (IFN-gamma)) mRNA expression, and macroscopic damage. Total gut permeability, MPO activity, and macroscopic damage were also assessed four days after intracolonic administration of 2,4,6-trinitrobenzenesulphonic acid (TNBS).
Results:
Maternal deprivation triggered a significant increase in colonic permeability associated with bacterial translocation into the mesenteric lymph nodes, liver, and spleen. These alterations were associated with some macroscopic damage and an increase in colonic MPO activity, mucosal mast cell density, and cytokine mRNA expression. Intracolonic infusion of TNBS induced a significantly higher inflammatory reaction in separated animals, as judged by enhanced MPO colonic levels, total gut permeability, and macroscopic lesions.
Conclusions:
Maternal deprivation promotes long term alterations in the colonic epithelial barrier associated with an exaggerated immune response to an external immune stimulus. This suggests a role for early psychological factors in the regulation of colonic mucosal barrier in later life.
