Multiomics reveals microbial metabolites as key actors in intestinal fibrosis in Crohn's disease

EMBO Mol Med. 2024 Oct;16(10):2427-2449. doi: 10.1038/s44321-024-00129-8. Epub 2024 Sep 13.

Abstract

Intestinal fibrosis is the primary cause of disability in patients with Crohn's disease (CD), yet effective therapeutic strategies are currently lacking. Here, we report a multiomics analysis of gut microbiota and fecal/blood metabolites of 278 CD patients and 28 healthy controls, identifying characteristic alterations in gut microbiota (e.g., Lachnospiraceae, Ruminococcaceae, Muribaculaceae, Saccharimonadales) and metabolites (e.g., L-aspartic acid, glutamine, ethylmethylacetic acid) in moderate-severe intestinal fibrosis. By integrating multiomics data with magnetic resonance enterography features, putative links between microbial metabolites and intestinal fibrosis-associated morphological alterations were established. These potential associations were mediated by specific combinations of amino acids (e.g., L-aspartic acid), primary bile acids, and glutamine. Finally, we provided causal evidence that L-aspartic acid aggravated intestinal fibrosis both in vitro and in vivo. Overall, we offer a biologically plausible explanation for the hypothesis that gut microbiota and its metabolites promote intestinal fibrosis in CD while also identifying potential targets for therapeutic trials.

Keywords: Crohn’s Disease; Fibrosis; Gut Microbiota; Magnetic Resonance Enterography; Metabolites.

MeSH terms

  • Adult
  • Animals
  • Crohn Disease* / metabolism
  • Crohn Disease* / microbiology
  • Crohn Disease* / pathology
  • Feces / microbiology
  • Female
  • Fibrosis*
  • Gastrointestinal Microbiome*
  • Humans
  • Intestines / microbiology
  • Intestines / pathology
  • Male
  • Metabolome
  • Metabolomics
  • Mice
  • Middle Aged
  • Multiomics