Effect of intestinal microecology on postnatal weight gain in very preterm infants in intensive care units

Ying-Xue Ding1, Shou-Ni Wang2, Hong Cui3

  • 1Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China. dingyingxue@ccmu.edu.cn.

Gut Pathogens
|August 2, 2021
PubMed

Insights

The intestinal microecology of very preterm infants differs between those with extrauterine growth retardation (EUGR) and normal growth. Gut bacteria diversity is insufficient and delayed in NICU infants, impacting postnatal weight gain.

Area of Science:

  • Neonatal Medicine
  • Microbiology
  • Pediatric Gastroenterology

Background:

  • Postnatal weight gain is critical for very preterm infants.
  • Intestinal microecology plays a role in infant growth and development.
  • Extrauterine growth retardation (EUGR) is a common complication in the neonatal intensive care unit (NICU).

Purpose of the Study:

  • To investigate the relationship between intestinal microecology and postnatal weight gain in very preterm infants.
  • To compare the gut microbiota composition between infants with EUGR and those with normal growth.

Main Methods:

  • A cohort of very preterm infants in the NICU was divided into EUGR and normal growth groups.
  • Infant growth was assessed at 2 and 4 weeks post-birth.
  • 16S ribosomal RNA (rRNA) high-throughput sequencing was used to analyze the gut microbiota composition from stool samples.

Main Results:

  • No significant differences in alpha or beta diversity of gut microbiota were observed between the groups at 2 or 4 weeks.
  • Specific bacterial taxa, including Streptococcaceae and Enterococcaceae, differed between groups at 2 weeks.
  • No Bifidobacterium was detected in either group at 4 weeks, indicating insufficient gut flora establishment.

Conclusions:

  • Intestinal microecology differs between very preterm infants with and without EUGR.
  • Preterm infants in the NICU exhibit insufficient gut microbiota diversity and richness.
  • Delayed establishment of intestinal homeostasis may contribute to impaired growth in this population.
Abstract