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Intestinal Microbiota Signatures Associated With Histological Liver Steatosis in Pediatric-Onset Intestinal Failure

Katri Korpela1, Annika Mutanen2, Anne Salonen1

  • 11 Department of Bacteriology and Immunology, Immunobiology Research Program, University of Helsinki, Helsinki, Finland.

JPEN. Journal of Parenteral and Enteral Nutrition
|May 3, 2015
PubMed

Insights

Intestinal microbiota changes in patients with intestinal failure (IF) are linked to liver disease. Specific bacteria like Proteobacteria and Lactobacilli correlate with liver steatosis and fibrosis in IF-associated liver disease (IFALD).

Area of Science:

  • Gastroenterology
  • Microbiology
  • Hepatology

Background:

  • Intestinal failure (IF)-associated liver disease (IFALD) is a primary cause of mortality in IF patients.
  • The relationship between intestinal microbiota and IFALD remains poorly understood.

Purpose of the Study:

  • To investigate the association between intestinal microbiota composition and IFALD in patients with IF.
  • To explore the correlation of specific microbial alterations with liver injury, inflammation, and disease characteristics.

Main Methods:

  • Culture-independent phylogenetic microarray analysis was employed to compare intestinal microbiota in IF patients (n=23) and healthy controls (n=58).
  • Microbiota profiles were correlated with histological liver injury, fecal inflammatory markers (MMP-9, calprotectin), and clinical data.

Main Results:

  • IF patients exhibited an overabundance of Lactobacilli, Proteobacteria, and Actinobacteria, with reduced diversity and richness of Clostridium clusters.
  • Proteobacteria were linked to liver steatosis, fibrosis, prolonged parenteral nutrition (PN), and inflammation.
  • Lactobacilli correlated with advanced steatosis and fibrosis, particularly after PN weaning, without associated inflammation.

Conclusions:

  • Intestinal microbiota composition is significantly associated with liver steatosis in IF, offering a better predictive value than PN duration or bowel length.
  • A proposed model suggests steatosis initiation during PN due to Proteobacteria-derived lipopolysaccharides, progressing post-PN with dominant Lactobacilli influencing lipid metabolism.
Abstract

Keywords:
LactobacilliProteobacterialiver diseaseparenteral nutritionshort bowel syndrome

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