Antibody to the E3 glycoprotein protects mice against lethal venezuelan equine encephalitis virus infection.

Six monoclonal antibodies were isolated that exhibited specificity for a furin cleavage site deletion mutant (V3526) of Venezuelan equine encephalitis virus (VEEV). These antibodies comprise a single competition group and bound the E3 glycoprotein of VEEV subtype I viruses but failed to bind the E3 glycoprotein of other alphaviruses. These antibodies neutralized V3526 virus infectivity but did not neutralize the parental strain of Trinidad donkey (TrD) VEEV.

Proinflammatory mediators of toxic shock and their correlation to lethality.

Bacterial exotoxins and endotoxins both stimulate proinflammatory mediators but the contribution of each individual toxin in the release of mediators causing lethal shock is incompletely understood. This study examines the cytokine response and lethality of mice exposed to varying doses of staphylococcal enterotoxin B (SEB) or lipopolysaccharide (LPS) and their combinations. In vivo, SEB alone induced moderate levels of IL-2 and MCP-1 and all mice survived even with a high dose of SEB (100 microg/mouse).

Critical timing, location and duration of glucocorticoid administration rescue mice from superantigen-induced shock and attenuate lung injury.

Bacterial superantigens, such as staphylococcal enterotoxin B (SEB), are major virulence factors implicated in the pathogenesis of toxic shock. In this study we investigated the efficacy of glucocorticoid therapy in preventing SEB-induced lethal shock initiated through the respiratory route in mice. Dexamethasone, a potent anti-inflammatory steroid, administrated intranasally on the first day, followed by intraperitoneal doses on the subsequent 4 days, was effective in attenuating SEB-induced hypothermia, and reduction in systemic and pulmonary proinflammatory mediator release.

Central roles for IL-2 and MCP-1 following intranasal exposure to SEB: a new mouse model.

Murine models for bacterial superantigens like staphylococcal enterotoxin B (SEB) have to date been rather cumbersome. The reasons include: (1) necessary use of potentiating agents such as actinomycin D, d-galactosamine, lipopolysaccharide (LPS), or viruses; (2) high toxin amounts required to elicit effects; and/or (3) generation of phenotypic-stable transgenic animals. Our study employed readily available C3H/HeJ (TLR4 negative, LPS-nonresponsive) mice with intranasal and intraperitoneal administration of low microgram quantities of SEB.