Shiga Toxin Pathogenesis in Escherichia coli Infections

Shiga toxin-producing Escherichia coli (STEC) are a leading cause of severe gastrointestinal illness and systemic complications worldwide. Central to STEC virulence is the production of Shiga toxins (Stx), AB5-type exotoxins that bind to globotriaosylceramide (Gb3) receptors on host cells. Following phage-mediated induction of stx genes under stress conditions, toxins are released into the intestinal lumen, where they traverse the epithelial barrier, enter the circulation and target microvascular endothelial cells, especially within the kidneys and central nervous system. Toxin binding triggers inhibition of ribosomal protein synthesis, leading to cell death, microvascular thrombosis and the characteristic lesions of haemolytic uraemic syndrome (HUS). The host immune response, including cytokine release and complement activation, amplifies endothelial injury and contributes to systemic inflammation. Recent advances have elucidated the molecular interplay between prophage induction pathways and toxin expression, the cellular mechanisms of toxin uptake and trafficking, and the role of immune cell subsets in systemic dissemination. These insights inform the development of targeted anti-virulence strategies, novel therapeutics and improved outbreak prevention measures, underscoring the global significance of understanding Shiga toxin pathogenesis.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Shiga Toxin Pathogenesis in Escherichia coli Infections publication trend

The graph below shows the total number of articles in shiga toxin pathogenesis in escherichia coli infections across all publications each year (not limited to Nature Index journals).

Technical terms

Shiga toxin (Stx): A family of potent bacterial exotoxins that inhibit protein synthesis by cleaving 28S rRNA, leading to cell death.

Haemolytic uraemic syndrome (HUS): A life-threatening condition characterised by microangiopathic haemolytic anaemia, thrombocytopenia and acute renal failure following Stx exposure.

Type III secretion system (T3SS): A syringe-like apparatus used by E. coli to inject effector proteins into host cells, facilitating colonisation and virulence.

Globotriaosylceramide (Gb3) receptor: A glycosphingolipid present on endothelial and epithelial cells that serves as the primary binding site for Shiga toxins.

Toll-like receptor 4 (TLR4): A pattern recognition receptor on immune cells that can mediate binding and internalisation of bacterial toxins or components.

References

1. A prophage encoded ribosomal RNA methyltransferase regulates the virulence of Shiga-toxin-producing Escherichia coli (STEC). Nucleic Acids Research (2023).
2. Evaluating the protective effects of Aurodox in a murine model of Shiga toxin-producing Escherichia coli. npj Antimicrobials and Resistance (2025).
3. Inhibition of tumour necrosis factor alpha by Etanercept attenuates Shiga toxin-induced brain pathology. Journal of Neuroinflammation (2025).
4. Monocytes serve as Shiga toxin carriers during the development of hemolytic uremic syndrome. Cellular & Molecular Biology Letters (2025).