Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A preestablished infection with the parasitic helminth, Schistosoma mansoni, significantly reduced the incidence and delayed the onset of experimental autoimmune encephalomyelitis (EAE) in C57BL/6J mice immunized with myelin oligodendrocyte glycoprotein (MOG)(35-55) peptide. The altered disease progression was not solely due to the induction of a strong Th2 response, since intraperitoneal injection of schistosome eggs did not affect disease development. MOG-specific gamma interferon (IFN-gamma), nitric oxide, and tumor necrosis factor alpha production by splenocytes was significantly reduced in schistosome-infected mice compared to uninfected mice. However, similar levels of interleukin-10 (IL-10) were produced in an antigen-specific manner, suggesting that the induction of antigen-specific responses was not inhibited. Analysis of in vivo cytokine production by real-time PCR indicated that IL-12p40, but not IFN-gamma, transcript levels were dramatically reduced in the spinal cords of schistosome-infected, MOG-immunized mice. Furthermore, analysis of the cellular composition of the spinal cords and brains revealed that a preestablished infection with S. mansoni decreased central nervous system (CNS) inflammation, particularly of macrophages and CD4 T cells. These results suggest that schistosomiasis may negatively regulate the onset of EAE by downregulating the production of proinflammatory cytokines and altering CNS inflammation.
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PMID:Schistosomiasis decreases central nervous system inflammation and alters the progression of experimental autoimmune encephalomyelitis. 1293 42

The incidences of schistosomiasis and multiple sclerosis (MS) are mutually exclusive worldwide suggesting that schistosomiasis may offer protection against the induction of the immune-mediated disease, MS. Recent studies using the mouse model of MS, experimental autoimmune encephalomyelitis, support a direct suppression of the onset of MS by chronic Schistosoma mansoni infection. Self-reactive Th1 but not Th2 responses develop in infected mice immunized with myelin oligodendrocyte glycoprotein albeit at reduced levels indicating that the induction of auto-reactive T cells is not abolished nor phenotypically altered. CNS infiltration by inflammatory cells, particularly macrophages, is significantly reduced in S. mansoni-infected, immunized mice compared to uninfected, immunized mice. Because activated macrophages are crucial to the induction of clinical disease, these findings support the hypothesis that differences in macrophage activation may contribute to the reduced incidence and delayed progression of experimental autoimmune encephalomyelitis during schistosomiasis.
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PMID:Schistosomiasis protects against multiple sclerosis. 1548 32

Multiple sclerosis (MS) is a common disabling autoimmune disease in young adults which does not have an effective treatment. The prevalence of immune-mediated diseases is higher in developed countries with hygienic environments, suggesting that helminthic infection may protect from autoimmune diseases. Previously, we reported that soluble egg antigens (SEA) from Schistosoma japonicum suppressed experimental autoimmune encephalomyelitis (EAE), an animal model of MS, through up-regulating T helper-2 (Th2) immune responses in both the peripheral and central target organs. Neurotrophins (NTs) are not exclusive to the nervous system. While immune cells, especially Th2 cells, can produce and secrete a variety of NTs resulting in neuroprotective immunity. NTs can also modulate immune responses by augmenting Th2 responses and downregulating Th1 responses. Interestingly, nerve growth factor (NGF) has been found in liver granulomas of Schistosoma mansoni-infected mice. Moreover, in the central nervous system of chronic schistosomiasis, NGF is increased. A hypothesis is hereby proposed - SEA derived from S. japonicum bears neuroprotective properties beyond its immunomodulatory effects. SEA can induce the expression of NTs, which in turn augment Th2 immune responses induced by SEA; whereby a positive regulatory circuit between Th2 responses and NTs comes into being.
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PMID:Neuroprotective potential beyond immunoregulation of helminth infection as a therapeutic target in multiple sclerosis. 2204 87