Linking E. coli to fibrosis in Crohn's disease

Ethan T Dehantschutter; Cormac T Taylor

doi:10.1016/j.chom.2024.12.011

Linking E. coli to fibrosis in Crohn's disease

Cell Host Microbe. 2025 Jan 8;33(1):12-14. doi: 10.1016/j.chom.2024.12.011.

Authors

Ethan T Dehantschutter¹, Cormac T Taylor²

Affiliations

¹ The Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland; UCD School of Medicine, University College Dublin, Dublin, Ireland.
² The Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland; UCD School of Medicine, University College Dublin, Dublin, Ireland. Electronic address: [email protected].

PMID: 39788093
DOI: 10.1016/j.chom.2024.12.011

Abstract

Intestinal fibrosis associated with Crohn's disease is a serious yet poorly understood clinical complication. In this issue of Cell Host & Microbe, Ahn and colleagues provide evidence that the adherent intestinal E. coli produced the metallophore yersiniabactin, which sequesters zinc to drive intestinal fibrosis in a HIF-1α-dependent manner.

MeSH terms

Animals
Crohn Disease* / complications
Crohn Disease* / microbiology
Crohn Disease* / pathology
Escherichia coli Infections / microbiology
Escherichia coli* / pathogenicity
Fibrosis*
Humans
Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
Intestinal Mucosa / microbiology
Intestinal Mucosa / pathology
Intestines / microbiology
Intestines / pathology
Phenols
Thiazoles
Zinc / metabolism

Substances

yersiniabactin
Zinc
Hypoxia-Inducible Factor 1, alpha Subunit
Phenols
Thiazoles