Abstract
Escherichia coli (EHEC) and Shigella dysenteriae serotype 1 are enterohemorrhagic bacteria that induce hemorrhagic colitis. This, in turn, may result in potentially lethal complications, such as hemolytic uremic syndrome (HUS), which is characterized by thrombocytopenia, acute renal failure, and neurological abnormalities. Both species of bacteria produce Shiga toxins (Stxs), a phage-encoded exotoxin inhibiting protein synthesis in host cells that are primarily responsible for bacterial virulence. Although most studies have focused on the pathogenic roles of Stxs as harmful substances capable of inducing cell death and as proinflammatory factors that sensitize the host target organs to damage, less is known about the interface between the commensalism of bacterial communities and the pathogenicity of the toxins. The gut contains more species of bacteria than any other organ, providing pathogenic bacteria that colonize the gut with a greater number of opportunities to encounter other bacterial species. Notably, the presence in the intestines of pathogenic EHEC producing Stxs associated with severe illness may have compounding effects on the diversity of the indigenous bacteria and bacterial communities in the gut. The present review focuses on studies describing the roles of Stxs in the complex interactions between pathogenic Shiga toxin-producing E. coli, the resident microbiome, and host tissues. The determination of these interactions may provide insights into the unresolved issues regarding these pathogens.
Highlights
This review summarizes the current understanding of the roles of E. coli Shiga toxins (Stxs) and Shiga-toxin-producing Escherichia coli (STEC) at their interfaces with commensal microbiota in the gut, mainly focusing on interactions with human microbiota
It is reported that the incubation of nonpathogenic phage-susceptible E. coli with toxinencoding phages resulted in up to a 40-fold greater production of toxin when compared with lysogens alone, suggesting that nonpathogenic phage-susceptible commensal E. coli may play a role in the pathogenesis of hemolytic uremic syndrome (HUS) [129]
Attempts to identify Stxs-induced risk factors in host cellular responses have revealed that these toxins have a wide range of novel properties that are associated with pathogenesis
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Stx-producing bacteria have received substantial attention as emergent pathogens due to the dangerous toxins they produce These exotoxins are the principal virulence factors associated with the pathogenesis of bloody diarrheal diseases, bacillary dysentery, and hemorrhagic colitis progressing to acute renal failure in infected patients, primarily in children. This phenomenon, collectively referred to as hemolytic uremic syndrome (HUS), is the leading cause of pediatric acute renal failure in many countries, including countries in the European Union and the United States [10,11]. This review summarizes the current understanding of the roles of E. coli Stxs and STEC at their interfaces with commensal microbiota in the gut, mainly focusing on interactions with human microbiota
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
