Why the study?
Does a PEGylated aptamer antagonist reduce mortality in a mouse model of SEB-induced toxic shock syndrome?
Does a PEGylated aptamer antagonist reduce mortality in a mouse model of SEB-induced toxic shock syndrome?
A novel aptamer antagonist against Staphylococcal enterotoxin B reduces mortality in a mouse model of toxic shock syndrome, suggesting potential therapeutic efficacy.
Hypothesis-generating for aptamer therapy in SEB toxic shock; warrants human trials before any clinical consideration.
Staphylococcal enterotoxin B (SEB) is a major virulence factor for staphylococcal toxic shock syndrome (TSS). SEB activates a large subset of the T lymphocytic population, releasing proinflammatory cytokines. Blocking SEB-initiated toxicity may be an effective strategy for treating TSS. Using a process known as systematic evolution of ligands by exponential enrichment (SELEX), we identified an aptamer that can antagonize SEB with nanomolar binding affinity (Kd = 64 nM). The aptamer antagonist effectively inhibits SEB-mediated proliferation and cytokine secretion in human peripheral blood mononuclear cells. Moreover, a PEGylated aptamer antagonist significantly reduced mortality in a "double-hit" mouse model of SEB-induced TSS, established via sensitization with d-galactosamine followed by SEB challenge. Therefore, our novel aptamer antagonist may offer potential therapeutic efficacy against SEB-mediated TSS.
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Wang et al. (2015) studied this question.
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