Abstract
Bile salts exhibit potent antibacterial properties, acting as detergents to disrupt cell membranes and as DNA-damaging agents. Although bacteria inhabiting the intestinal tract are able to resist bile’s antimicrobial effects, relatively little is known about how bile influences virulence of enteric pathogens. Escherichia coli O157:H7 is an important pathogen of humans, capable of causing severe diarrhea and more serious sequelae. In this study, the transcriptome response of E. coli O157:H7 to bile was determined. Bile exposure induced significant changes in mRNA levels of genes related to virulence potential, including a reduction of mRNA for the 41 genes making up the locus of enterocyte effacement (LEE) pathogenicity island. Bile treatment had an unusual effect on mRNA levels for the entire flagella-chemotaxis regulon, resulting in two- to four-fold increases in mRNA levels for genes associated with the flagella hook-basal body structure, but a two-fold decrease for “late” flagella genes associated with the flagella filament, stator motor, and chemotaxis. Bile salts also caused increased mRNA levels for seventeen genes associated with iron scavenging and metabolism, and counteracted the inhibitory effect of the iron chelating agent 2,2’-dipyridyl on growth of E. coli O157:H7. These findings suggest that E. coli O157:H7 may use bile as an environmental signal to adapt to changing conditions associated with the small intestine, including adaptation to an iron-scarce environment.
Highlights
Bacteria must resist the antimicrobial properties of bile in order to survive in the small intestine [1]
We describe an O157:H7 transcriptome associated with bile and how bile may be affecting the virulence properties of the bacteria prior to intestinal colonization
A human-associated strain of O157:H7 was grown for three hours in the presence or absence of 0.8% bile salts
Summary
Bacteria must resist the antimicrobial properties of bile in order to survive in the small intestine [1]. Bile salts act as a biological detergent that aids in digestion through emulsification of fatty foods. These detergent properties allow bile to disrupt the membranes of bacteria. Bile salts act as DNAdamaging agents [2] and can cause oxidative stress [3]. Bacteria that have adapted to life in the intestine have developed mechanisms of resistance to bile, including modified membrane structures that reduce bile permeability, and efflux pumps that are able to transport bile out of the cell [1]. Bile has been proposed to be a signal to enteric pathogens of having entered the small intestine and for the regulated expression of virulence [4].
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