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Published on: July 28, 2022
Neonatal hypoxia leads to impaired intestinal function and changes in the composition and metabolism of its
Jun Wen1, Yue Wu1, Fengfeng Zhang1
1Institute of Developmental and Regenerative Biology, Zhejiang Key Laboratory of Organ Development and Regeneration, College of Life and Environmental Sciences, Hangzhou Normal University, NO.2318, Yuhangtang Rd, Yuhang District, Hangzhou, 311121, PR China.
Insights
Neonatal hypoxia damages the newborn intestine, causing structural changes and altering gut bacteria. This may impact metabolic and neurological health in infants.
Area of Science:
- Neonatal physiology
- Gastroenterology
- Microbiology
Background:
- Neonatal hypoxia is a common perinatal complication impacting newborn health.
- The neonatal intestine is highly susceptible to hypoxic injury due to its metabolic activity.
Purpose of the Study:
- To investigate hypoxia-induced intestinal barrier damage in a neonatal mouse model.
- To elucidate the underlying mechanisms, including structural, genetic, and microbial changes.
Main Methods:
- Utilized a neonatal hypoxic mouse model.
- Performed histological analysis (F4/80+ cells, tight junctions, mucus particles).
- Analyzed gene expression related to intestinal barrier function.
- Conducted 16S rDNA sequencing for gut microbiota analysis.
Main Results:
- Hypoxia induced significant intestinal structural abnormalities (ileum, colon), including inflammation and disrupted tight junctions.
- Gene expression related to barrier function, immunity, motility, and absorption was dysregulated.
- Gut microbiota exhibited dysbiosis, with reduced microbial abundance and diversity.
- Microbiota changes correlated with perturbed metabolic homeostasis, particularly glycolipid metabolism.
Conclusions:
- Neonatal hypoxia severely compromises intestinal barrier integrity and function.
- Hypoxia-induced gut dysbiosis contributes to metabolic disturbances.
- Potential links between hypoxia, gut microbiota, and neurological disorders warrant further investigation.
Abstract:
Neonatal hypoxia, a prevalent complication during the perinatal period, poses a serious threat to the health of newborns. The intestine, as one of the most metabolically active organs under stress conditions, is particularly vulnerable and susceptible to hypoxic injury. Using a neonatal hypoxic mouse model, we systematically investigated hypoxia-induced intestinal barrier damage and underlying mechanisms. Hypoxia caused significant structural abnormalities in the ileum and distal colon of neonatal mice, including increased numbers of F4/80+ cells (p = 0.0031), swollen mucus particles (p = 0.0119), and disrupted tight junction. At the genetic level, hypoxia caused dysregulation of the expression of genes involved in intestinal barrier function, including antimicrobial activity, immune response, intestinal motility, and nutrient absorption. Further 16 S rDNA sequencing revealed hypoxia-driven gut microbiota dysbiosis with general reduced microbial abundance and diversity (Chao1 = 0.1143, Shannon = 0.0571, and Simpson = 0.3429). Structural dysbiosis of the gut microbiota consequently perturbed metabolic homeostasis, especially enhancing the activity of glycolipid metabolism. Notably, results showed that hypoxia may interfere with neurotransmitter metabolism, thereby increasing the risk of neurological disorders.
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