Given that etanercept can be used to successfully treat SJS/TEN and TNF-alpha levels are elevated in TSS, if a dermatologist chooses to treat TEN with etanercept, consideration of TSS on the differential should not necessarily exclude etanercept as a reasonable treatment option.
Although intact TSST1 causes lethal shock in vivo, the individual domains of this molecule may have therapeutic potential: the N-terminal domain to antagonize lymphocyte activation and TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimulate antitumor responses without MHC II binding.
Major histocompatibility complex (MHC) class II engagement by toxic shock syndrome toxin 1 (TSST-1) transduces signals leading to proinflammatory cytokine gene expression (tumor necrosis factor alpha [TNF-alpha]) in human monocytes.
To allow rapid identification of toxic shock syndrome toxin-1 (TSST-1)-producing Staphylococcus aureus strains, a real-time PCR assay for the detection of the tst gene, which encodes TSST-1, was developed.
Three hundred and thirty-two strains isolated from ten provinces between June 1999 and January 2002 were characterized by staphylococcal enterotoxin genes, toxic shock syndrome toxin 1 (tst) gene, and exfoliative toxin genes.
A rapid and specific assay for toxic shock syndrome toxin-1 gene (tst gene) detection in Staphylococcus aureus was developed using the polymerase chain reaction.
Even if Panton-Valentine leukocidin (PVL), toxic shock syndrome toxin-1 (TSST-1), staphylococcal enterotoxins (SEB and SEC), and exfoliative toxins (ETA and ETB) may be associated with severe infections, the clinical significance of their presence in clinical isolates of Staphylococcus aureus remains poorly documented.
The DVbetaS of TSST-1 and SEB were detected in patients with menstrual and non-menstrual TSS, respectively, whereas no Vbeta signature was detected during septic shock.
Antibiotic susceptibility, biofilm formation, Staphylococcal protein A (spa) typing, SCCmec typing, and PCR-based assays were used to detect mecA, mecC, vanA, Panton-Valentine Leukocidin toxin (PVL), and toxic shock syndrome toxin-1 (tst) genes.
The isolates did not display any consistent virulence gene pattern, and 35 % of the isolates carried at least one of the Panton-Valentine leukocidin (lukFS-PV), exfoliative toxin (eta) or toxic shock syndrome (tst) genes.
Important characteristics, e.g., carriage of the enterotoxin A (sea) and toxic shock syndrome toxin (tst) genes and production of urease, are described.
However, unlike the classical enterotoxins SEB and toxic shock syndrome toxin 1 (TSST-1), the gene for SEl-K is commonly present in more than half of all Staphylococcus aureus clinical isolates and is present in almost all USA300 community-acquired methicillin-resistant S. aureus (CA-MRSA) isolates.
TSST-1 was better able to stimulate chemokine (IL-8 and MIP-3α) production by HVECs than SEB and SEC, suggesting this is the reason for TSST-1's exclusive association with menstrual TSS.
The majority of the clones responded to at least one of the SA tested, staphylococcal enterotoxins (SEA and SEB) and toxic shock syndrome toxin-1 (TSST-1).
The majority of the clones responded to at least one of the SA tested, staphylococcal enterotoxins (SEA and SEB) and toxic shock syndrome toxin-1 (TSST-1).
The strain produced the enterotoxin SEA and the toxic shock syndrome toxin-1, and was also found to exhibit the genes encoding enterotoxins SEG and SEI, as well as the enterotoxin gene cluster egc.
We report a single fusion protein (TBA<sub>225</sub>) consisting of the toxoid versions of TSST-1, SEB and SEA and demonstrate its immunogenicity and protective efficacy in a mouse model of toxic shock.
Interleukin-10 (IL-10) Produced by Mutant Toxic Shock Syndrome Toxin 1 Vaccine-Induced Memory T Cells Downregulates IL-17 Production and Abrogates the Protective Effect against Staphylococcus aureus Infection.
The third objective was to assess IL-10 responses to endotoxin and toxic shock syndrome toxin (TSST) from leukocytes of smokers and non-smokers in relation to the IL-10 (G-1082A) polymorphism.
Our data demonstrate a novel mechanism of immunopathology in which CD8(+) T cells mediate Ehrlichia-induced toxic shock, which is associated with IL-10 overproduction and CD4(+) T-cell apoptosis.
Interleukin-10 (IL-10) Produced by Mutant Toxic Shock Syndrome Toxin 1 Vaccine-Induced Memory T Cells Downregulates IL-17 Production and Abrogates the Protective Effect against Staphylococcus aureus Infection.
Furthermore, interfering with IL-17A receptor signaling in human PBMCs attenuated the expression of numerous inflammatory mediators implicated in the TSS-associated cytokine storm.