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.
Highlights
The adherent-invasive Escherichia coli (AIEC) pathogroup was initially characterized in isolates from the ileal mucosa of Crohn’s disease (CD) patients[1,2,3,4,5]
We identified the most highly expressed genes, i.e., those showing an increase of at least 4-fold in mRNA abundance in bacteria grown with bile salts in comparison to bacteria grown without bile salts
Global RNA sequencing (RNA-seq) of AIEC reference strain LF82 has been used to decipher the impact of bile salts on the expression of metabolic bacterial genes
Summary
The adherent-invasive Escherichia coli (AIEC) pathogroup was initially characterized in isolates from the ileal mucosa of Crohn’s disease (CD) patients[1,2,3,4,5] These bacteria strongly adhere to and invade intestinal epithelial cells (IECs), survive within macrophages, move into the deep tissues and activate immune cells to induce inflammatory cytokine secretion[6,7,8]. A huge body of literature has provided evidence that most enteropathogens are equipped with a large set of specific metabolic pathways to overcome nutritional limitations in vivo, increasing bacterial fitness during infection[14] These adaptations include the degradation of myo-inositol, ethanolamine cleaved from phospholipids, fucose derived from mucosal glycoconjugates, 1,2-propanediol as the fermentation product of fucose or rhamnose and several other metabolites not accessible for commensal bacteria or present in competition-free microenvironments. We showed that secondary metabolic pathways in AIEC are modulated by bile salts, providing them with energy as well as carbon and nitrogen sources to colonize the intestinal mucosa
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