biostudies-literatureUnknown59(4)Wang KStaphylococcal 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 Antimicrobial agents and chemotherapy2072-7https://www.ebi.ac.uk/biostudies/studies/S-EPMC4356834biostudies-literatureNeutralization of staphylococcal enterotoxin B by an aptamer antagonist.PMC4356834Yang XJiang LGan LChen MZhang XLan XWang KfalseNeutralization of staphylococcal enterotoxin B by an aptamer antagonist.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 2015-01-01T00:00:00Z2015 Apr2025-04-19T23:57:10.085Z2019-03-27T01:48:02ZS-EPMC43568342562432510.1128/AAC.04414-1410.1128/aac.04414-14