Metabolic adaptation of adherent-invasive Escherichia coli to exposure to bile salts

Sci Rep. 2019 Feb 18;9(1):2175. doi: 10.1038/s41598-019-38628-1.

Abstract

The adherent-invasive Escherichia coli (AIEC), which colonize the ileal mucosa of Crohn's disease patients, adhere to intestinal epithelial cells, invade them and exacerbate intestinal inflammation. The high nutrient competition between the commensal microbiota and AIEC pathobiont requires the latter to occupy their own metabolic niches to survive and proliferate within the gut. In this study, a global RNA sequencing of AIEC strain LF82 has been used to observe the impact of bile salts on the expression of metabolic genes. The results showed a global up-regulation of genes involved in degradation and a down-regulation of those implicated in biosynthesis. The main up-regulated degradation pathways were ethanolamine, 1,2-propanediol and citrate utilization, as well as the methyl-citrate pathway. Our study reveals that ethanolamine utilization bestows a competitive advantage of AIEC strains that are metabolically capable of its degradation in the presence of bile salts. We observed that bile salts activated secondary metabolism pathways that communicate to provide an energy benefit to AIEC. Bile salts may be used by AIEC as an environmental signal to promote their colonization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetyl Coenzyme A / metabolism
  • Adaptation, Physiological
  • Animals
  • Bacterial Adhesion
  • Bile Acids and Salts / pharmacology*
  • Crohn Disease / microbiology
  • Escherichia coli / drug effects*
  • Escherichia coli / genetics
  • Escherichia coli / metabolism*
  • Escherichia coli Infections / microbiology
  • Ethanolamine / metabolism
  • Gastrointestinal Microbiome / drug effects
  • Gastrointestinal Microbiome / genetics
  • Genes, Bacterial / drug effects
  • Host Microbial Interactions / drug effects
  • Humans
  • Ileum / microbiology
  • Intestinal Mucosa / microbiology
  • Metabolic Networks and Pathways / drug effects
  • Metabolic Networks and Pathways / genetics
  • Mice
  • Mice, Inbred C57BL
  • Propylene Glycol / metabolism
  • Up-Regulation / drug effects

Substances

  • Bile Acids and Salts
  • Ethanolamine
  • Propylene Glycol
  • Acetyl Coenzyme A