Ethanolamine Influences Human Commensal <named-content content-type="genus-species">Escherichia coli</named-content> Growth, Gene Expression, and Competition with Enterohemorrhagic <named-content content-type="genus-species">E. coli</named-content> O157:H7

Abstract

ABSTRACT A core principle of bacterial pathogenesis is that pathogens preferentially utilize metabolites that commensal bacteria do not in order to sidestep nutritional competition. The metabolite ethanolamine (EA) is well recognized to play a central role in host adaptation for diverse pathogens. EA promotes growth and influences virulence during host infection. Although genes encoding EA utilization have been identified in diverse bacteria (nonpathogenic and pathogenic), a prevailing idea is that commensal bacteria do not utilize EA to enhance growth, and thus, EA is a noncompetitive metabolite for pathogens. Here, we show that EA augments growth of two human commensal strains of Escherichia coli. Significantly, these commensal strains grow more rapidly than, and even outcompete, the pathogen enterohemorrhagic E. coli O157:H7 specifically when EA is provided as the sole nitrogen source. Moreover, EA-dependent signaling is similarly conserved in the human commensal E. coli strain HS and influences expression of adhesins. These findings suggest a more extensive role for EA utilization in bacterial physiology and host-microbiota-pathogen interactions than previously appreciated. IMPORTANCE 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-microbiota-pathogen interactions.

Keywords

• ethanolamine
• metabolism
• microbiota
• signaling