Staphylococcal enterotoxin B increased severity of experimental model of multiple sclerosis

Superantigens can be absorbed trans-mucosal and trans-cutaneous in individuals colonized with superantigen producing Staphylococcus aureus. Ability of superantigens to activate a large numbers of T cells suggests that they may play a role in the course of autoimmune diseases including human multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). In this study we investigated the role of staphylococcal enterotoxin B in immunologic and pathologic changes in experimental animal model of multiple sclerosis.

C57BL/6 female mice were treatment with SEB protein prior or post immunization with MOG_33-35 peptide. Mice were monitored daily and scored for clinical symptoms following EAE induction. Spleen and spinal cord of mice were removed and used for ELISA and histological studies, respectively.

Treatment with SEB prior induction of EAE, increased clinical score, the concentration of IL-17A, IFN-γ and histological changes compared to control group. Treatment with SEB after induction of EAE caused these changes, but less severe.

Since SEB causes demyelination of spinal cord and increases the level of pro-inflammatory cytokine response, infiltration of T-lymphocytes and macrophages to CNS, it may exacerbate the clinical signs of EAE in mice and multiple sclerosis in human.