Abstract
The microbiota protects the host from invading pathogens by limiting
access to nutrients. In turn, bacterial pathogens selectively exploit metabolites
not readily used by the microbiota to establish infection. Ethanolamine has been
linked to pathogenesis of diverse pathogens by serving as a noncompetitive metabolite that enhances pathogen growth as well as a signal that modulates virulence. Although ethanolamine is abundant in the gastrointestinal tract, the prevailing idea is that commensal bacteria do not utilize EA, and thus, EA utilization has been particularly associated with pathogenesis. Here, we provide evidence that two human commensal Escherichia coli isolates readily utilize ethanolamine to enhance growth, modulate gene expression, and outgrow the pathogen enterohemorrhagic E. coli. These data indicate a more complex role for ethanolamine in host-microbiotapathogen interactions.
access to nutrients. In turn, bacterial pathogens selectively exploit metabolites
not readily used by the microbiota to establish infection. Ethanolamine has been
linked to pathogenesis of diverse pathogens by serving as a noncompetitive metabolite that enhances pathogen growth as well as a signal that modulates virulence. Although ethanolamine is abundant in the gastrointestinal tract, the prevailing idea is that commensal bacteria do not utilize EA, and thus, EA utilization has been particularly associated with pathogenesis. Here, we provide evidence that two human commensal Escherichia coli isolates readily utilize ethanolamine to enhance growth, modulate gene expression, and outgrow the pathogen enterohemorrhagic E. coli. These data indicate a more complex role for ethanolamine in host-microbiotapathogen interactions.
| Original language | English |
|---|---|
| Journal | mBio |
| Volume | 9 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - 2 Oct 2018 |