Gut Microbiota Profile Changes in Patients with Inflammatory Bowel Disease and Non-Alcoholic Fatty Liver Disease: A Metagenomic Study

Int J Mol Sci. 2024 May 17;25(10):5453. doi: 10.3390/ijms25105453.

Abstract

Gut microbiota imbalances have a significant role in the pathogenesis of Inflammatory Bowel Disease (IBD) and Non-Alcoholic Fatty Liver Disease (NAFLD). Herein, we compared gut microbial composition in patients diagnosed with either IBD or NAFLD or a combination of both. Seventy-four participants were stratified into four groups: IBD-NAFLD, IBD-only, NAFLD-only patients, and healthy controls (CTRLs). The 16S rRNA was sequenced by Next-Generation Sequencing. Bioinformatics and statistical analysis were performed. Bacterial α-diversity showed a significant lower value when the IBD-only group was compared to the other groups and particularly against the IBD-NAFLD group. β-diversity also showed a significant difference among groups. The higher Bacteroidetes/Firmicutes ratio was found only when comparing IBD groups and CTRLs. Comparing the IBD-only group with the IBD-NAFLD group, a decrease in differential abundance of Subdoligranulum, Parabacteroides, and Fusicatenibacter was found. Comparing the NAFLD-only with the IBD-NAFLD groups, there was a higher abundance of Alistipes, Odoribacter, Sutterella, and Lachnospira. An inverse relationship in the comparison between the IBD-only group and the other groups was shown. For the first time, the singularity of the gut microbial composition in IBD and NAFLD patients has been shown, implying a potential microbial signature mainly influenced by gut inflammation.

Keywords: IBD; NAFLD; gut microbiota; leaky gut; liver steatosis.

MeSH terms

  • Adult
  • Bacteria / classification
  • Bacteria / genetics
  • Bacteria / isolation & purification
  • Female
  • Gastrointestinal Microbiome* / genetics
  • Humans
  • Inflammatory Bowel Diseases* / microbiology
  • Male
  • Metagenome
  • Metagenomics* / methods
  • Middle Aged
  • Non-alcoholic Fatty Liver Disease* / genetics
  • Non-alcoholic Fatty Liver Disease* / microbiology
  • RNA, Ribosomal, 16S* / genetics

Substances

  • RNA, Ribosomal, 16S

Grants and funding

This research received no external funding.