Abstract
Background: Accumulating evidence suggests a connection between the gut microbiota and neonatal diseases. Hypoxia may play an important role in the intestinal lesions in neonates.Objective: This study aims to determine whether the gut microbiota differs between intrauterine hypoxic rats and healthy controls and to identify the factors that influence the changes in the gut microbiota.Methods: We constructed an intrauterine hypoxia model in rats and collected the intestinal contents of intrauterine hypoxic newborn rats and normal newborn rats within 4 h and on the seventh day after birth. They were divided them into the intrauterine hypoxia first-day group (INH1), intrauterine hypoxia seventh-day group (INH7), normal first-day group (NOR1), and normal seventh-day group (NOR7). The contents of the intestines were sequenced with 16S rRNA sequencing, the sequencing results were analyzed for biological information, and the differences in the diversity, richness, and individual taxa among the groups were analyzed.Results: The abundance of the gut microbiota of neonatal rats with intrauterine hypoxia was higher than that of the control group rats. Intrauterine hypoxia altered the structural composition of the gut microbiota in neonatal rats. The INH1 group showed increased species richness, phylogenetic diversity, and β-diversity, and altered relative abundance in several taxa compared to those in the control group. The differences in the microbiota among the four groups were significantly higher than those within the group, and the differences in the abundance and diversity of the INH7 and NOR7 groups decreased after 7 days of suckling. Functional analysis based on the Cluster of Orthologous Groups (COG) suggested that 23 functional COG categories. There was no significant difference in the functional categories between the hypoxia group and the normal group.Conclusion: Intrauterine hypoxia changed the initial colonization of the gut microbiota in neonatal rats. It could increase the species richness and β-diversity of the gut microbiota, and altered relative abundances of several taxa.
Highlights
Intrauterine hypoxia is a prevalent problem in fetuses and neonates, and it is one of the important causes leading to fetal intrauterine distress, growth restriction, hypoxic-ischemic encephalopathy of neonates, and even fetal and neonatal death
One group of rats was stimulated with hypoxia after conception to construct an intrauterine hypoxia model as the experimental group, and the other group was treated as the control group without any intervention after conception
Rats in the hypoxia group weighed significantly less than rats in the normal group (p < 0.05) (Figure 1)
Summary
Intrauterine hypoxia is a prevalent problem in fetuses and neonates, and it is one of the important causes leading to fetal intrauterine distress, growth restriction, hypoxic-ischemic encephalopathy of neonates, and even fetal and neonatal death. Necrotizing enterocolitis (NEC) is a catastrophic disease that is a major cause of mortality in preterm infants who survive the first few days after birth [4]. Formula feeding, abnormal bacterial colonization, and intestinal barrier dysfunction have been identified as the main etiological factors that substantially potentiate the risk of NEC [4]. The damage to the intestinal barrier is considered to be the most predominant cause of NEC in neonates. As one of the major pathological factors for infant intestines suffering from NEC [12], hypoxia induces cell death, and deterioration of the integrity of the intestinal barrier, thereby reducing the restorative ability of crypt stem cells [13]. Hypoxia may play an important role in the intestinal lesions in neonates
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