Related Experiment Video
Updated: Mar 29, 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
Antepartum Antibiotic Treatment Increases Offspring Susceptibility to Experimental Colitis: A Role of the Gut
Peris Mumbi Munyaka1,2, N Eissa1, Charles Noah Bernstein3,4
1Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
Insights
Antepartum antibiotic exposure in mice increased offspring susceptibility to colitis by altering gut microbiota composition and function. This suggests potential long-term health implications for children born to mothers receiving antibiotics during pregnancy.
Area of Science:
- Microbiome research
- Immunology
- Gastroenterology
Background:
- Postnatal immune system maturation relies on microbial exposure.
- Gut colonization patterns may influence childhood diseases persisting into adulthood.
Purpose of the Study:
- To investigate if antepartum antibiotic (ATB) therapy increases offspring susceptibility to experimental colitis.
- To determine if ATB therapy alters the gut microbiota, contributing to disease susceptibility.
Main Methods:
- Pregnant mice received cefazolin or saline antepartum.
- Offspring (7 weeks old) were exposed to dextran sulfate sodium (DSS) to induce colitis.
- Gut microbiota composition (16S rRNA sequencing) and inflammatory markers (IL-6, IL-1β, CRP) were analyzed.
Main Results:
- Antepartum antibiotics altered fecal bacterial composition and predicted functional pathways.
- Antibiotic exposure increased colitis severity, histologic damage, and colonic IL-6 levels in offspring.
- Microbial richness decreased, and composition shifted in fecal and colonic samples post-antibiotic exposure.
Conclusions:
- Antepartum antibiotics modulate offspring gut microbiota, increasing susceptibility to colonic inflammation.
- Findings support the hypothesis in a murine colitis model.
- Results may inform interventions to restore healthy gut colonization in infants exposed to maternal antibiotics.
Background And Aims:
Postnatal maturation of the immune system is largely driven by exposure to microbes, and thus the nature of intestinal colonization may be associated with development of childhood diseases that may persist into adulthood. We investigated whether antepartum antibiotic (ATB) therapy can increase offspring susceptibility to experimental colitis through alteration of the gut microbiota.
Methods:
Pregnant C57Bl/6 mice were treated with cefazolin at 160 mg/kg body weight or with saline starting six days before due date. At 7 weeks, fecal samples were collected from male offspring after which they received 4% dextran sulfate sodium (DSS) in drinking water for 5 days. Disease activity index, histology, colonic IL-6, IL-1β and serum C-reactive protein (CRP) were determined. The V3-V4 region of colonic and fecal bacterial 16S rRNA was sequenced. Alpha-, beta-diversity and differences at the phylum and genus levels were determined, while functional pathways of classified bacteria were predicted.
Results:
ATB influenced fecal bacterial composition and hence bacterial functional pathways before induction of colitis. After induction of colitis, ATB increased onset of clinical disease, histologic score, and colonic IL-6. In addition, ATB decreased fecal microbial richness, changed fecal and colon microbial composition, which was accompanied by a modification of microbial functional pathways. Also, several taxa were associated with ATB at lower taxonomical levels.
Conclusions:
The results support the hypothesis that antepartum antibiotics modulate offspring intestinal bacterial colonization and increase susceptibility to develop colonic inflammation in a murine model of colitis, and may guide future interventions to restore physiologic intestinal colonization in offspring born by antibiotic-exposed mothers.
More Related Videos
09:09Generating a Reproducible Model of Mid-Gestational Maternal Immune Activation using PolyI:C to Study Susceptibility and Resilience in Offspring
Published on: August 17, 2022
07:34Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
Published on: December 16, 2021