ArticleJournal of advanced research2026
Prenatal supplementation with the gut-derived tryptophan metabolite indole-3-propionic acid alleviates colitis susceptibility in maternal immune-activated offspring mice.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- ROS-responsive hydrogel delivering liposomal indole-3-propionic acid promotes spinal cord injury repair by enhancing CX3CL1-CX3CR1 mediated neuron-microglia communication.Materials today. Bio · 2026Article
- Gut microbiota‑immune crosstalk in recurrent pregnancy loss: Mechanisms and therapeutic perspectives (Review).Molecular medicine reports · 2026Review
- Maternal and infant gut microbiome.iMeta · 2026Review
- The Impact of Oral-Gut Microbiota Structure and Its Manipulation on RA Development and Management.Food science & nutrition · 2026Review
- Epigenetic Perspectives on Maternal Gut Microbiota's Impact on Embryonic and Fetal Development.Comprehensive Physiology · 2026Review
- 6-Bromoindole-3-acetonitrile Attenuates DSS-Induced Colitis by Inhibiting Epithelial Cell Pyroptosis.Foods (Basel, Switzerland) · 2026Article
- Microbial regulation of intestinal stem cell function: implications for alleviating intestinal injury of weaned piglets.NPJ biofilms and microbiomes · 2026Review
- Gut Metabolite Indoleacrylic Acid Suppresses Osteoclast Formation by AHR mediated NF-κB Signaling Pathway.International journal of biological sciences · 2026Article
- Mechanisms by which tryptophan metabolites enhance intestinal barrier function to prevent necrotizing enterocolitis in preterm infants.Frontiers in immunology · 2026Review
- Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD.EBioMedicine · 2026Article
- Pediococcus acidilactici attenuates chronic stress-induced depression via generating metabolite indole-3-lactic acid and downregulating neuroinflammation.Journal of neuroinflammation · 2025Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMaternal immune activation (MIA) impairs gut immune function in offspring, with maternal microbiota and their metabolites influencing intestinal development. Indole-3-propionic acid (IPA), a microbial metabolite derived from tryptophan, promotes gut health by enhancing epithelial proliferation. However, the impact of prenatal IPA supplementation on offspring gut outcomes remains unclear.
objectivesThis study investigated whether prenatal IPA supplementation could mitigate the susceptibility of MIA offspring to colitis.
methodsPregnant mice received oral IPA (20 mg/kg body weight) from embryonic day 5.5 (E5.5) until delivery, with MIA induced at E12.5. Female offspring (7-8 weeks old) were exposed to 3.5 % dextran sulfate sodium (DSS)-induced colitis. IPA levels were measured in maternal serum and amniotic fluid at E14.5 to assess maternal-fetal transfer and potential effects on fetal gut development.
resultsPrenatal IPA supplementation attenuated colitis severity in MIA offspring, as evidenced by reduced body weight loss, milder diarrhea, lower disease activity index, and diminished colonic damage, along with alleviation of anxiety-like behavior. Moreover, prenatal IPA supplementation decreased serum and colonic proinflammatory factor levels and improved colonic barrier function following DSS-induced colitis. Additionally, prenatal IPA supplementation enhanced the proportion of beneficial gut microbiota, such as Bifidobacterium, Lactobacillus, Limosilactobacillus, Allobaculum, and Faecalibaculum, which contributed to intestinal epithelial cell growth and helped preserve barrier integrity. Notably, IPA can be transferred from the mother to the fetus through blood and amniotic fluid, facilitating the mRNA expression of Mdr1b, Ctnnb1, and Lgr5, which are involved in gut cell proliferation and differentiation.
conclusionPrenatal IPA is transferred to the fetus and promotes gut development, conferring long-term protection against colitis in MIA offspring. These findings underscore the enduring impact of maternal interventions on offspring intestinal health.
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