Abstract
Among the toxin family of bacterial superantigens, the six members of the enterotoxin gene cluster (egc) seem to have unusual characteristics. They are present in the majority of Staphylococcus aureus strains, but their role in disease remains uncertain. We assessed secretion levels, immunogenicity, and toxicity of native and recombinant egc proteins. After having developed enzyme-linked immunosorbent assays, we found different quantities of egc proteins secreted by bacterial isolates. Supernatants induced proliferation of human peripheral blood mononuclear cells. However, purified recombinant egc proteins were shown to have differing superantigenicity potentials. Immunization with identical amounts of all members of egc, and the prominent toxic agent SEB, resulted in neutralizing antisera. Two egc proteins, SEI and SElN, were found to play a predominant role within the cluster. Both displayed the highest potential to activate blood cells, and were essential to be neutralized in supernatants. The application of a supernatant of a strain bearing only egc was sufficient for a lethal outcome in a rabbit model. Again, neutralization of SEI and SElN led to the survival of all tested animals. Finally, nanogram amounts of purified rSEI and rSElN led to lethality in vivo, pointing out the importance of both as virulence determinants among egc superantigens.
Highlights
Staphylococcus aureus is known to be one of the most challenging human bacterial pathogens worldwide
We investigated the characteristics of a colonizing isolate having seb and seh beside the egc gene cluster (Table 1)
Induction of proliferation was quantified by Strikingly, we found that the dual combination of antisera against was sufficient peripheral blood mononuclear cells (MNC)
Summary
Staphylococcus aureus is known to be one of the most challenging human bacterial pathogens worldwide. We know of a number of examples of secreted and membrane-associated proteins of S. aureus, which are believed to contribute to distinct disease patterns. This arsenal includes hydrolytic enzymes, adhesins, and a large number of toxins, such as superantigens [3,4,5]. A large group of T cells are activated through a cascade initiated by the binding of superantigens to MHC class II and the Vβ chains of the T cell receptor. This mechanism leads to toxic shock syndrome (TSS) [7]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: 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.