<i>Staphylococcus aureus</i> is a pathogen that causes severe infectious diseases that eventually lead to septic and toxic shock.<i>S. aureus</i> infection is characterized by the production of virulence factors, including enzymes and toxins.After internalization <i>S. aureus</i> resides in a phagosome labeled with Rab7 protein.Here, we show that <i>S. aureus</i> generates tubular structures marked with the small GTPases Rab1b and Rab7 and by the autophagic protein LC3 at early times post-infection.
<i>Staphylococcus aureus</i> is a pathogen that causes severe infectious diseases that eventually lead to septic and toxic shock.<i>S. aureus</i> infection is characterized by the production of virulence factors, including enzymes and toxins.After internalization <i>S. aureus</i> resides in a phagosome labeled with Rab7 protein.Here, we show that <i>S. aureus</i> generates tubular structures marked with the small GTPases Rab1b and Rab7 and by the autophagic protein LC3 at early times post-infection.
<i>Staphylococcus aureus</i> is a pathogen that causes severe infectious diseases that eventually lead to septic and toxic shock.<i>S. aureus</i> infection is characterized by the production of virulence factors, including enzymes and toxins.After internalization <i>S. aureus</i> resides in a phagosome labeled with Rab7 protein.Here, we show that <i>S. aureus</i> generates tubular structures marked with the small GTPases Rab1b and Rab7 and by the autophagic protein LC3 at early times post-infection.
Toll-like receptor 2-independent host innate immune response against an epidemic strain of Streptococcus suis that causes a toxic shock-like syndrome in humans.
M protein is the most abundant GAS surface protein, and M1 serotype GAS strains are associated with invasive infections, including necrotizing fasciitis and toxic shock syndrome.
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.
A comprehensive analysis of Staphylococcus aureus superantigen (SAG) genes was undertaken in isolates from a major hospital and compared with isolates from patients with toxic shock syndrome (TSS).
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.
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.
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.
Cases hospitalized with S. aureus infections at the University General Hospital of Patras, Greece, during a 4-year period (2013-2016) were studied. mecA, lukS/lukF-PV (Panton-Valentine leukocidin, PVL), tst (toxic shock syndrome toxin), fnbA (fibronectin-binding protein A), eta, and etb (epidermolytic toxins) genes' carriage was detected by PCR in 149 selected patients.
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.
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.
Functional analysis of the TCR binding domain of toxic shock syndrome toxin-1 predicts further diversity in MHC class II/superantigen/TCR ternary complexes.
Furthermore, interfering with IL-17A receptor signaling in human PBMCs attenuated the expression of numerous inflammatory mediators implicated in the TSS-associated cytokine storm.