Previous infection with Staphylococcus aureusstrains attenuated experimental encephalomyelitis

Abstract

BackgroundBacterial superantigens are potent T cell activators that can activate T cells with specificity for antigens of the central nervous system (CNS). In this study, we compared the effect of two S. aureus strains on experimental autoimmune encephalomyelitis (EAE) development. C57BL/6 female mice were infected with S. aureus ATCC 51650, which produces toxic shock syndrome toxin 1 (TSST-1+) or S. aureus ATCC 43300, which does not produce toxins (TOX-). Three days later, the animals were subjected to EAE induction by immunization with myelin oligodendrocyte glycoprotein (MOG). The weight variation, disease incidence and clinical score were recorded daily. Cytokines and Foxp3+ regulatory T cells in the brain were evaluated during the acute disease phase. Cytokines and Foxp3+ regulatory T cells in the spleen and histopathological analysis of the CNS were assessed during the chronic stage.ResultsPrevious infection with both strains similarly decreased the clinical score; however, only the TSST-1+ strain clearly diminished inflammation in the CNS. The infections also modulated cytokine production in the spleen and CNS. Reduced production of IL-5 and IL-10 was detected in MOG-stimulated spleen cultures in the TOX- and TSST-1+ infected groups, respectively. In S. aureus stimulated cultures, there was an increased production of IFN-γ and IL-10 in both infected groups and an increased level of IL-5 in the TSST-1+ group. CNS infiltrating cell cultures from previously infected mice produced less IL-17 in response to MOG and more IFN-γ in response to S. aureus stimulation.ConclusionsThese results indicated that both strains attenuated clinical EAE manifestations, but only TSST-1 clearly decreased CNS inflammation.

RETRACTED ARTICLE: Resistant Strains of Enterotoxigenic Staphylococcus aureus; Unknown Risk for Multiple Sclerosis Exacerbation

“…The total prevalence of sea , seb , sec , sed , seg and sei genes in the S. aureus isolates of MS exacerbation patients were 30%, 11.11%, 15.55%, 4.44%, 1.11% and 1.11%, respectively. Higher prevalence of superantigens and enterotoxigenic genes, in the patients who suffered from MS, were reported previously by Mulvey et al ( 4 ), Franca et al ( 7 ) and Kumar et al ( 27 ).…”

“…Enterotoxigenic genes of the S. aureus can activate a high proportion of T cells, due to their ability to bind to both major histocompatibility complex (MHC) molecules in antigen presenting cells and specific V-β regions, in the T cell receptor ( 4 , 7 ). This activation results in the polyclonal stimulation of T cells and an increased production of proinflammatory cytokines ( 4 , 7 ). Based on the controversial theories and the results of previous studies, the enterotoxigenic genes of S. aureus may be involved in the fundamental etiology of multiple sclerosis (MS).…”

“…Based on the controversial theories and the results of previous studies, the enterotoxigenic genes of S. aureus may be involved in the fundamental etiology of multiple sclerosis (MS). The MS is a chronic disease of the central nervous system, with incompletely known etiology ( 4 , 7 - 9 ). It is widely accepted as a complex autoimmune disease, generally targeting young adults ( 10 ).…”

Oral infection with P. gingivalis exacerbates autoimmune encephalomyelitis

“…27 This indicates that the effect of infection on EAE development is associated with either acute or chronic inflammatory responses. It is interesting to note that recent data failed to show exacerbation of EAE severity by other infections: Franca et al 32 showed that preceding infection with Staphylococcus aureus actually decreases EAE clinical scores; Another study showed that infection with Taenia crassiceps also led to attenuation of EAE. 33 In both studies, the infections led to Th2 immunologic characteristics response.…”

Association of myelin peptide with vitamin D prevents autoimmune encephalomyelitis development

“…Experimental autoimmune encephalomyelitis (EAE) has been extensively used to elucidate the pathophysiology and the potential therapeutic measures applied to MS (Franc¸a et al, 2014;Zorzella-Pezavento et al, 2014;Rahimi et al, 2015). Current therapeutic approaches to control the destructive immune response in autoimmune disease are mainly based on non-specific drugs that systemically suppress the function of many immune effector cells.…”