Abstract
Background and aimsPostnatal 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.MethodsPregnant 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.ResultsATB 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.ConclusionsThe 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.
Highlights
The use of antibiotics during pregnancy or around the time of delivery is a common practice in clinical settings in North America, more so due to the fear of newborn colonization with Group B streptococci (GBS) during passage through the birth canal or when the membranes rapture
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
Pre-partum antibiotics are generally recommended for premature rupture of membranes or when vaginal colonization by group B streptococci is detected, antibiotics are frequently used in other clinical situations in which a clear benefit has not been demonstrated [4], and this has raised some concerns [5]
Summary
The use of antibiotics during pregnancy or around the time of delivery is a common practice in clinical settings in North America, more so due to the fear of newborn colonization with Group B streptococci (GBS) during passage through the birth canal or when the membranes rapture. Perinatal antibiotics may influence the initial microbial colonization of the newborn intestine, which is essential for the normal host development,[7] since the early neonatal period represents the most important opportunity for microbiota-induced hosthomeostasis [8]. Postnatal maturation of the immune system is largely driven by exposure to microbes, and 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
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