Effect of viral infection on experimental allergic encephalomyelitis in mice

Wu, Linxian; Mäkelä, Mika; Röyttä, Matias; Salmi, A.

doi:10.1016/0165-5728(88)90062-8

Cited by 21 publications

(10 citation statements)

References 28 publications

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“…Infection is also associated with an autoimmune response to myelin [86] and for patients with established MS, infection may result in an exacerbation or disease relapse [87]. A putative role for TLR2 in the aggravation of the disease by infection has been demonstrated using EAE in TLR2 -/-mice; the TLR2 -/-mice were protected from a Streptococcus pneumoniae-induced exacerbation [88].…”

Section: Multiple Sclerosismentioning

confidence: 95%

Modulation of toll-like receptor function has therapeutic potential in autoimmune disease

Clanchy¹,

Sacre

2010

Expert Opinion on Biological Therapy

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As initiators of immune responses, TLRs have previously been targeted to increase the immune response with some success. However, targeting TLRs to attenuate immune responses for the treatment of chronic inflammatory diseases will require further evidence of the mechanisms of TLR involvement in the pathophysiology and a better understanding of the potential effects of modulating TLR physiology over a sustained period.

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Section: Multiple Sclerosismentioning

confidence: 95%

Modulation of toll-like receptor function has therapeutic potential in autoimmune disease

Clanchy¹,

Sacre

2010

Expert Opinion on Biological Therapy

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“…It has been reported that LPS rendered B10.A mice susceptible to the development of post-infectious autoimmune myocarditis by Coxsackie virus B3 (CB3) infection [27], possibly through promoting the production of TNF and/or IL-1 [28,29]. Mokhtarian & Swoveland [30] reported that predisposing C57BL/J mice with a non-fatal strain of Semliki Forest virus facilitated the induction of experimental autoimmune encephalomyelitis (EAE), and Wu et al [5] found that the infection of BALB/c and SJL/J mice with SFV-A7 virus could either inhibit or facilitate the development of EAE, depending on whether the virus was injected before or after the EAE induction. The mechanisms underlying these interactions remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…An avirulent mutant strain of Semliki Forest virus (SFV-A7) was obtained from Dr H. E. Webb (Neurology Unit, Department of Neurology, Rayne Institute, St Thomas' Hospital, London, UK). The virus was propagated in a mouse brain cell line-MBA-13 [5]. Virus stocks were titrated by a standard plaque assay method and aliquots stored at ¹70ЊC.…”

Section: Methodsmentioning

confidence: 99%

“…In this respect IL-2 and IL-1 are probably important, since IL-2 supports T cell development, and its production is influenced by IL-1, a major pro-inflammatory cytokine with pleiotropical properties [32,33]. Further studies of the cytokine expression following SFV-A7 infection in vivo may provide more direct insight into the pathogenesis of SFV-A7 modulated EAE, an animal model for human multiple sclerosis [5,30].…”

Section: Semliki Forest Virus and Lps Induce Il-1b And Il-2 Expressiomentioning

confidence: 99%

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Altered IL‐1β and IL‐2 mRNA Expression in Murine Splenic Cells After Concomitant Stimulation by Semliki Forest Virus and Lipopolysaccharide

et al. 1997

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Yang J, Hukkanen V, Seljelid R, Salmi AA. Altered IL-1b and IL-2 mRNA Expression in Murine Splenic Cells After Concomitant Stimulation by Semliki Forest Virus and Lipopolysaccharide. Scand J Immunol 1997;45:349-353 Co-infection with virus and bacteria happens frequently and often results in an exacerbated clinical course of the disease, possibly due to mechanisms including altered cytokine production. In the present study, the authors investigated the combined effects of avirulent Semliki Forest virus (SFV-A7) and bacterial lipopolysaccharide (LPS) on the interleukin-1b (IL-1b) and IL-2 gene expression in murine splenic cells. The authors found that 10 ng/ml of LPS in the culture medium induced expression of IL-1b but not IL-2, while infection with SFV-A7 did not induce either of these two cytokines. However, when SFV-A7 and LPS were applied together, a synergistic increase of both IL-1b and IL-2 was observed. Further experiments showed that addition of SFV-A7 3 h before LPS enhanced, whereas addition of the virus 3 h after the LPS inhibited, IL-1b gene expression. These results indicate that an interaction of virus and Gram-negative bacteria can result in an altered cytokine gene expression.

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“…Similar to the findings in humans, viral infections are important triggering factors for the animal model of MS, experimental autoimmune encephalomyelitis (EAE). Examples are Semliki Forest virus or gammaherpesvirus infections, which can strongly evoke relapses (25,48).…”

mentioning

confidence: 99%

Streptococcus pneumoniaeInfection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2

et al. 2006

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The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG 35-55 ) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG 35-55 injection but was more severe in animals infected 7 days after the first MOG 35-55 injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

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Effect of viral infection on experimental allergic encephalomyelitis in mice

Cited by 21 publications

References 28 publications

Modulation of toll-like receptor function has therapeutic potential in autoimmune disease

Modulation of toll-like receptor function has therapeutic potential in autoimmune disease

Altered IL‐1β and IL‐2 mRNA Expression in Murine Splenic Cells After Concomitant Stimulation by Semliki Forest Virus and Lipopolysaccharide

Streptococcus pneumoniaeInfection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2

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