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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #411892
Research Project: Intestinal Microbial Ecology and Non-Antibiotic Strategies to Limit Shiga Toxin-Producing Escherichia coli (STEC) and Antimicrobial Resistance Transmission in Food Animals

Location: Food Safety and Enteric Pathogens Research

Title: Differential expression of virulence genes in Shiga toxin-producing Escherichia coli O157:H7 during initial colonization of human colonic epithelial and rectoanal junction cells revealed host-specific Adaptations

Author
item EDISON, LEKSHMI - University Of Florida
item Kudva, Indira
item KARIYAWASAM, SUBHASHINIE - University Of Florida

Submitted to: American Society for Microbiology
Publication Type: Abstract Only
Publication Acceptance Date: 2/28/2024
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Shiga toxin-producing Escherichia coli (STEC) is a major foodborne pathogen. Cattle, is the primary reservoir and asymptomatic carriers, harbor the pathogen predominantly in their rectoanal junction (RAJ), serving as a pivotal source of food contamination. Despite the importance of cattle in STEC transmission to humans, the molecular mechanisms governing its adaptation in the RAJ and subsequent infection of human colonic epithelial cells leading to diarrhea remain largely unexplored. Understanding the host-specific strategies employed by STEC during early colonization is crucial for unraveling the intricacies of pathogenesis. This study explores the complex dynamics of STEC O157:H7 in two host environments—bovine RAJ cells and human colonic epithelial cells—during initial colonization. Utilizing comparative transcriptomics analysis, we investigated differential gene expression profiles of STEC O157:H7 during initial interaction with these cell types. STEC O157:H7 was cultured with bovine RAJ cells and the human colonic epithelial cell line CCD CoN 841 to simulate STEC and intestinal epithelial cell interactions. High-throughput RNA sequencing insights into the molecular responses of STEC O157:H7, which showed 829 and 1939 bacterial genes expressed in RAJ and CCD CoN 841 cells, respectively. After gene filtering, 221 genes were upregulated during initial adherence to CCD CoN cells and 436 with RAJ cells. Furthermore, 22 genes were uniquely expressed during interaction with human cells and 155 genes with bovine cells. Our results indicated a remarkable divergence in the expression profiles of virulence genes between the two host environments. Specifically, ten virulence genes, including those within the chu iron transport locus (chuA, chuS, chuY) and the shu heme utilization locus (shuU, shuT), as well as genes associated with enterobactin biosynthesis (entF, ybdZ), high-affinity ferric uptake (fhuE), and iron uptake and assimilation (efeB, efeO), were upregulated during initial adherence to CCD CON 841. Contrastingly, these same virulence genes were downregulated during adherence to RAJ cells. The present study also identified seven virulence genes, including espW, wzb, iraD, purC, purD, and narG, demonstrating higher expression in bovine cells than in human cells. This investigation might advances our understanding of the nuanced dynamics involved in STEC colonization in different host microenvironments and providing valuable avenues for developing novel interventions to mitigate human STEC foodborne infections.