DIFFERENTIAL EFFECTS OF EPINEPHRINE, NOREPINEPHRINE, AND INDOLE ON Escherichia coli O157:H7 CHEMOTAXIS, COLONIZATION, AND GENE EXPRESSION

Artie McFerrin Department of Chemical Engineering, Texas A&M University, College Station, TX 77843-3122

^* To whom correspondence should be addressed. Email: arulj{at}tamu.edu.

	Abstract

During infection in the gastrointestinal (GI) tract, Escherichia coli O157:H7 (EHEC) is exposed to a wide range of signaling molecules, including the eukaryotic hormones epinephrine and norepinephrine, and bacterial signal molecules such as indole. Since these signaling molecules have been shown to be involved in the regulation of phenotypes such as motility and virulence that are crucial for EHEC infections, we hypothesized that these molecules also govern the initial recognition of the large intestine environment and attachment to the host cell surface. Here, we report that epinephrine and norepinephrine exert divergent effects on EHEC chemotaxis, motility, biofilm formation, gene expression, and colonization of HeLa cells, as compared to indole. Using a novel two flourophore chemotactic assay, it was found that EHEC is attracted towards epinephrine and norepinephrine while it is repelled by indole. In addition, epinephrine and norepinephrine also increased EHEC motility and biofilm formation while indole attenuated these phenotypes. DNA microarray analysis of surface-associated EHEC indicated that epinephrine/norepinephrine up-regulated the expression of genes involved in surface colonization and virulence while exposure to indole decreased their expression. The gene expression data also suggested that AI-2 uptake was repressed upon exposure to epinephrine/norepinephrine but not indole. In vitro adherence experiments confirmed that epinephrine and norepinehrine increase attachment to epithelial cells while indole decreased adherence. Taken together, these results suggest that epinephrine and norepinephrine increase EHEC infection while indole attenuates the process.