Staphylococcal Enterotoxin B Increased Severity of Experimental Model of Multiple Sclerosis Publisher Pubmed



Pakbaz Z¹ ; Sahraian MA² ; Noorbakhsh F³ ; Salami SA⁴ ; Pourmand MR¹
Source: Microbial Pathogenesis Published:2020

Abstract

Background: 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. Methods: C57BL/6 female mice were treatment with SEB protein prior or post immunization with MOG33-35 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. Results: 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. Discussion: 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. © 2020 Elsevier Ltd