Murine Lethal Toxic Shock Caused by Intranasal Administration of Staphylococcal Enterotoxin B

ABSTRACT Staphylococcal enterotoxin B induces toxic shock and is a major virulence factor of staphylococcal diseases. We examined the effects of systemic adenoviral infection on responses to staphylococcal enterotoxin B in a murine model. We found that adenoviral infection markedly increases the severity of liver injury following exposure to staphylococcal enterotoxin B without d-galactosamine sensitization. In adenovirus-infected mice, staphylococcal enterotoxin B triggered a more profound hypothermia and increased apoptosis in the liver. Consistent with these observations, we also found that adenoviral infection primed for an increased production of gamma interferon in vivo and in vitro following stimulation with staphylococcal enterotoxin B. Gamma-interferon-knockout mice did not show increased sensitivity to staphylococcal enterotoxin B following adenoviral infection. These data suggest that a preexisting viral infection primes mice for subsequent staphylococcal enterotoxin B exposure, possibly via a gamma-interferon-mediated mechanism.

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Neutralization of Staphylococcal Enterotoxin B by an Aptamer Antagonist

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.04414-14 ◽

2015 ◽

Vol 59 (4) ◽

pp. 2072-2077 ◽

Cited By ~ 19

Author(s):

Kaiyu Wang ◽

Longjie Gan ◽

Li Jiang ◽

Xianhui Zhang ◽

Xiangyue Yang ◽

...

Keyword(s):

Mononuclear Cells ◽

Human Peripheral Blood ◽

Staphylococcal Enterotoxin ◽

Staphylococcal Enterotoxin B ◽

Toxic Shock ◽

Peripheral Blood Mononuclear ◽

Systematic Evolution ◽

Enterotoxin B ◽

Staphylococcal Toxic Shock Syndrome ◽

Exponential Enrichment

ABSTRACTStaphylococcal 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 withd-galactosamine followed by SEB challenge. Therefore, our novel aptamer antagonist may offer potential therapeutic efficacy against SEB-mediated TSS.

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Detection of Staphylococcal Enterotoxin B and toxic shock syndrome toxin: PCR versus conventional methods

Zentralblatt für Bakteriologie ◽

10.1016/s0934-8840(11)80706-1 ◽

1995 ◽

Vol 282 (4) ◽

pp. 367-371 ◽

Cited By ~ 5

Author(s):

F. Schumacher-Perdreau ◽

A. Akatova ◽

G. Pulverer

Keyword(s):

Toxic Shock Syndrome ◽

Staphylococcal Enterotoxin ◽

Staphylococcal Enterotoxin B ◽

Toxic Shock ◽

Enterotoxin B ◽

Conventional Methods ◽

Toxic Shock Syndrome Toxin

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Rapamycin Protects Mice from Staphylococcal Enterotoxin B-Induced Toxic Shock and Blocks Cytokine Release InVitro and In Vivo

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01015-09 ◽

2010 ◽

Vol 54 (3) ◽

pp. 1125-1131 ◽

Cited By ~ 30

Author(s):

Teresa Krakauer ◽

Marilyn Buckley ◽

Haleem J. Issaq ◽

Stephen D. Fox

Keyword(s):

Mononuclear Cells ◽

Human Peripheral Blood ◽

Staphylococcal Enterotoxin ◽

Staphylococcal Enterotoxin B ◽

Toxic Shock ◽

Peripheral Blood Mononuclear ◽

Necrosis Factor Alpha ◽

Enterotoxin B

ABSTRACT Staphylococcal enterotoxins are potent activators for human T cells and cause lethal toxic shock. Rapamycin, an immunosuppressant, was tested for its ability to inhibit staphylococcal enterotoxin B (SEB)-induced activation of human peripheral blood mononuclear cells (PBMC) in vitro and toxin-mediated shock in mice. Stimulation of PMBC by SEB was effectively blocked by rapamycin as evidenced by the inhibition of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), IL-6, IL-2, gamma interferon (IFN-γ), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and T-cell proliferation. In vivo, rapamycin protected 100% of mice from lethal shock, even when administered 24 h after intranasal SEB challenge. The serum levels of MCP-1 and IL-6, after intranasal exposure to SEB, were significantly reduced in mice given rapamycin versus controls. Additionally, rapamycin diminished the weight loss and temperature fluctuations elicited by SEB.

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