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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 #409051

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: Comparative transcriptome analysis of Shiga toxin-producing Escherichia coli O157:H7 on bovine rectoanal junction cells and human colonic epithelial cells during initial adherence

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

Submitted to: Microorganisms
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/11/2023
Publication Date: 10/15/2023
Citation: Edison, L.K., Kudva, I.T., Kariyawasam, S. 2023. Comparative transcriptome analysis of Shiga toxin-producing Escherichia coli O157:H7 on bovine rectoanal junction cells and human colonic epithelial cells during initial adherence. Microorganisms. 11(10). Article 2562.

Interpretive Summary: Cattle asymptomatically carry Shiga toxin-producing Escherichia coli (STEC) that can cause severe disease in humans, in their intestinal tracts. A specific region of the bovine intestinal tract found near the rectum, referred to as the rectoanal junction (RAJ), serves as the primary site for STEC attachment and persistence. In humans, STEC infection can result in extended tissue damage in the colon region of the intestine leading to symptoms ranging from diarrhea to toxin-induced systemic failures. Understanding the molecular mechanisms that allow STEC to adapt to the bovine RAJ without disease yet subsequently infect the human colon remains largely unexplored. To begin to understand differences in STEC behavior between the two environments, differences in STEC gene expression during its interaction with the cells at the bovine RAJ and human colon was evaluated. Our findings identified differences in STEC gene expression in response to cues from the different host cells, underscoring versatile strategies used by STEC for colonization, survival, and potentially causing disease. These results contribute to a deeper understanding of STEC behavior in specific host contexts, as well as provides a foundation for future research aimed at deciphering its colonization and pathogenic mechanisms in different host niches to develop targeted interventions to mitigate STEC in both cattle and humans.

Technical Abstract: Shiga toxin-producing Escherichia coli (STEC) are notorious foodborne pathogens capable of causing severe diarrhea and other life-threatening complications in humans. Cattle remain a major reservoir and asymptomatic carriers of STEC. In reservoir animals, the rectoanal junction (RAJ) serves as the primary colonization site of STEC playing a critical role in its transmission to humans through contaminated food sources. However, the molecular mechanisms behind the adaptation of STEC in the RAJ of the asymptomatic reservoir host and its subsequent infection of human colonic epithelial cells in an event of a foodborne transmission to cause diarrhea remain largely unexplored. This study aimed to unravel the intricate dynamics of STEC O157:H7 serotype in these two distinct host environments: bovine RAJ cells and human colonic epithelial cells, during initial colonization. In this context, comparative transcriptomics analysis was employed to investigate the differential gene expression profiles of STEC O157:H7 during its interaction with these cell types. The bacterial cells were cultured under controlled conditions to simulate the microenvironments of both bovine RAJ and human colonic epithelial cells. Using high throughput RNA sequencing, we identified key bacterial genes and regulatory pathways that were significantly modulated in response to each specific host environment. Our findings reveal distinct expression patterns of bacterial genes involved in virulence, including adherence, metal iron homeostasis and stress response in STEC O157:H7 grown in bovine RAJ cells as opposed to human colonic epithelial cells six hours post-infection. Additionally, the comparative analysis highlights the potential role of certain genes in host adaptation and tissue-specific pathogenicity. Furthermore, this study sheds light on the potential factors contributing to the survival and persistence of STEC O157:H7 in the bovine reservoir, and its ability to colonize intestinal epithelium and cause disease in humans.