Abstract

Foodborne pathogens are a public health threat globally. Shiga toxin-producing Escherichia coli (STEC), particularly O26, O111, and O157 STEC, are often associated with foodborne illness in humans. To create effective preharvest interventions, it is critical to understand which factors STEC strains use to colonize the gastrointestinal tract of cattle, which serves as the reservoir for these pathogens. Several colonization factors are known, but little is understood about initial STEC colonization factors. Our objective was to identify these factors via contrasting gene expression between nonpathogenic E. coli and STEC. Colonic explants were inoculated with nonpathogenic E. coli strain MG1655 or STEC strains (O26, O111, or O157), bacterial colonization levels were determined, and RNA was isolated and sequenced. STEC strains adhered to colonic explants at numerically but not significantly higher levels compared to MG1655. After incubation with colonic explants, flagellin (fliC) was upregulated (log2 fold-change = 4.0, p < 0.0001) in O157 STEC, and collectively, Lon protease (lon) was upregulated (log2 fold-change = 3.6, p = 0.0009) in STEC strains compared to MG1655. These results demonstrate that H7 flagellum and Lon protease may play roles in early colonization and could be potential targets to reduce colonization in cattle.

Highlights

  • Shiga toxin-producing Escherichia coli (STEC) strains are gastrointestinal pathogens that cause mild to severe bloody diarrhea in humans [1]

  • The proposed timeline of STEC adherence begins with initial interaction with the extracellular membrane [30], which was the focus of our study

  • STEC strains adhered at numerically higher levels, no significant differences were detected between the strains

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Summary

Introduction

Shiga toxin-producing Escherichia coli (STEC) strains are gastrointestinal pathogens that cause mild to severe bloody diarrhea in humans [1]. Clinical disease caused by STEC infections can occur in humans at any age, but children less than five years old are susceptible [3]. 15% of STEC infections will progress to the severe disease, hemolytic uremic syndrome [4]. Common sources of human infection include contaminated foods such as beef, dairy, and produce [7]. The reduction of these pathogens in animals, food processing plants, and elimination from food products is important for protecting public health [8]

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