[Features of intestinal flora in children with food protein-induced proctocolitis based on high-throughput

Shun-Li Chen1, Zheng-Zhen Tang, Bo Huang

  • 1Graduate School of Zunyi Medical University, Zunyi, Guizhou 563000, China.

Insights

Infants with food protein-induced proctocolitis (FPIP) exhibit altered gut microbiota, with reduced diversity and specific bacterial genus changes. These dysbiotic shifts may contribute to FPIP development.

Area of Science:

  • Microbiology
  • Pediatric Gastroenterology
  • Gut Microbiome Research

Background:

  • Food protein-induced proctocolitis (FPIP) is an allergic condition in infants.
  • The gut microbiome plays a crucial role in infant health and immune development.
  • Understanding FPIP-associated gut dysbiosis is essential for developing targeted interventions.

Purpose of the Study:

  • To investigate the characteristics of the intestinal flora in infants diagnosed with FPIP.
  • To compare the gut microbiome composition between FPIP infants and healthy controls.
  • To identify specific bacterial taxa associated with FPIP.

Main Methods:

  • A case-control study involving 31 infants with FPIP and 31 healthy controls (<6 months old).
  • High-throughput sequencing of 16S rDNA V3-V4 fragments from fecal samples.
  • Bioinformatic analysis to assess microbial diversity and composition at phylum and genus levels.

Main Results:

  • Infants with FPIP showed reduced microbial diversity (Shannon index) but increased abundance (Chao index) compared to controls.
  • FPIP group exhibited a significant decrease in Actinobacteria and an increase in Proteobacteria at the phylum level.
  • Key genus-level alterations in FPIP included reduced Bifidobacterium and Ruminococcus, and increased Clostridium and Shigella.

Conclusions:

  • FPIP is associated with decreased gut microbial diversity and altered bacterial abundance.
  • Specific changes in bacterial genera, such as Bifidobacterium and Clostridium, are linked to FPIP.
  • Gut dysbiosis at the genus level may be a significant factor in the pathogenesis of FPIP.
Abstract