Shiga toxin-producing Escherichia coli antigens and Shiga toxins (STEC antigens and Stx) (STEC antigens and Stx)

Shiga toxin-producing Escherichia coli (STEC) antigens and Shiga toxins (Stx) are the primary virulence factors responsible for severe foodborne illnesses, including hemorrhagic colitis and hemolytic uremic syndrome (HUS) (NIH, 2020). The Shiga toxins, categorized into Stx1 and Stx2, are AB5-type ribosome-inactivating proteins that bind to the globotriaosylceramide (Gb3) receptor on host endothelial cells, particularly in the kidneys and central nervous system (Wikipedia, 2024). Once internalized, the A-subunit of the toxin cleaves the 28S ribosomal RNA, halting protein synthesis and triggering apoptosis (Frontiers in Cellular and Infection Microbiology, 2020). STEC also utilizes surface antigens such as intimin (encoded by the eae gene) and the type III secretion system to adhere to and colonize the intestinal epithelium (NIH, 2020).\n\nTherapeutic strategies targeting these molecules include the development of monoclonal antibodies, such as Shigamabs and Urtoxazumab, which aim to neutralize circulating toxins (NIH, 2020). Toxin-sequestering agents like SYNSORB Pk have also been explored to bind toxins within the gut (NIH, 2020). A significant safety concern in treating STEC infections is the use of certain antibiotics, like fluoroquinolones, which can trigger the bacterial SOS response and lead to increased toxin production and release, thereby elevating the risk of HUS (Journal of Infectious Diseases, 2000). Consequently, management often relies on supportive care and the avoidance of toxin-inducing agents (NIH, 2020).

Other names

Verocytotoxin-producing Escherichia coliVTECEnterohemorrhagic Escherichia coliEHECShiga-like toxinsSLTVerotoxinsStx1Stx2IntiminO-antigenH-antigen

Neutralization of Shiga toxins (Stx1 and Stx2) to prevent binding to the host Gb3 receptor, inhibition of bacterial colonization through targeting surface antigens like intimin, and sequestration of toxins within the intestinal lumen. Some therapeutic approaches also involve inhibiting the bacterial SOS response to prevent the induction and release of toxin-encoding bacteriophages.