Resistance to experimental autoimmune encephalomyelitis development in Lewis rats from a conventional animal facility

Zorzella, Sofia Fernanda Gonçalves; Seger, Juliana; Martins, Denizar Cruz; Pelizon, A. C.; Sartori, Alexandrina

doi:10.1590/s0074-02762007000800007

Cited by 11 publications

(10 citation statements)

References 32 publications

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“…MBP-immunized animals reached maximal neurological deficits (EAE-score of 3-4) around 12-14 days after immunization, with a full recovery afterwards as described in various studies [44][45][46]. No significant difference in IOP between immunized groups and controls could be observed at any point in time.…”

Section: Assessment Of Clinical Parameterssupporting

confidence: 53%

Ophthalmopathology in rats with MBP-induced experimental autoimmune encephalomyelitis

Gramlich

Joachim²,

Gottschling

et al. 2011

Graefes Arch Clin Exp Ophthalmol

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Immunization with MBP not only causes neuron loss in the retinal ganglion cell layer, but also triggers antibody reactivity against ocular tissue. Possibly some of these antibodies are involved in the induction of neuronal apoptosis. This study suggests that, apart from T-cell mediation, alteration of antibody reactivity and activated microglia do also influence the ocular pathomechanisms in the EAE model.

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Section: Assessment Of Clinical Parameterssupporting

confidence: 53%

Ophthalmopathology in rats with MBP-induced experimental autoimmune encephalomyelitis

Gramlich

Joachim²,

Gottschling

et al. 2011

Graefes Arch Clin Exp Ophthalmol

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“…More subtle exposures to environmental microbes also appear to influence disease outcomes in various rodent autoimmune disease models. For example, animals housed in specific pathogen-free facilities vs conventional facilities appear to develop more severe EAE (8). However, this phenomenon is in contrast to myelin basic protein (MBP) TCR-transgenic animals, which develop spontaneous EAE under conventional but not specific pathogen-free conditions (9).…”

mentioning

confidence: 99%

Early Life Exposure to Lipopolysaccharide Suppresses Experimental Autoimmune Encephalomyelitis by Promoting Tolerogenic Dendritic Cells and Regulatory T Cells

Ellestad

Tsutsui

Noorbakhsh

et al. 2009

The Journal of Immunology

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The rising incidence of autoimmune diseases such as multiple sclerosis (MS) in developed countries might be due to a more hygienic environment, particularly during early life. To investigate this concept, we developed a model of neonatal exposure to a common pathogen-associated molecular pattern, LPS, and determined its impact on experimental autoimmune encephalomyelitis (EAE). Mice exposed to LPS at 2 wk of age showed a delayed onset and diminished severity of myelin oligodendrocyte glycoprotein (MOG)-induced EAE, induced at 12 wk, compared with vehicle-exposed animals. Spinal cord transcript levels of CD3ε and F4/80 were lower in LPS- compared with PBS-exposed EAE animals with increased IL-10 levels in the LPS-exposed group. Splenic CD11c+ cells from LPS-exposed animals exhibited reduced MHC class II and CD83 expression but increased levels of CD80 and CD86 both before and during EAE. MOG-treated APC from LPS-exposed animals stimulated less T lymphocyte proliferation but increased expansion of CD4+FoxP3+ T cells compared with APC from PBS-exposed animals. Neuropathological studies disclosed reduced myelin and axonal loss in spinal cords from LPS-exposed compared with PBS-exposed animals with EAE, and this neuroprotective effect was associated with an increased number of CD3+FoxP3+ immunoreactive cells. Analyses of human brain tissue revealed that FoxP3 expression was detected in lymphocytes, albeit reduced in MS compared with non-MS patients’ brains. These findings support the concept of early-life microbial exposure influencing the generation of neuroprotective regulatory T cells and may provide insights into new immunotherapeutic strategies for MS.

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“…EAE data provide a rationale for oral tolerance as a good therapeutic approach to the modulation of existing innate tolerance [Peron et al, 2010]. Susceptibility to EAE is affected by animal housing conditions and specific gut infections [Ochoa-Repáraz et al, 2009;Zorzella et al, 2007].…”

Section: Experimental Autoimmune Encephalomylitis: New Insightsmentioning

confidence: 99%

Innate origins of multiple sclerosis pathogenesis: Implications for computer‐assisted design of disease‐modifying therapies

Stoy

2011

Drug Development Research

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The rational development of disease-modifying therapies for multiple sclerosis (MS) requires a detailed knowledge of disease pathogenesis, but this remains incomplete. Dynamic computerassisted modeling of MS is currently hindered by uncertainties about the connectivity, compartmentalization, and dynamic sequencing of the components of the disease process. The present work presents a simple but versatile model of the mammalian immune system, incorporating both innate and adaptive immunity and innate and adaptive tolerance. The model is applied to MS and its animal model, experimental autoimmune encephalomyelitis (EAE), to interrogate the concept of initiation of MS lesions through activation of the peripheral innate immune system, triggering auto-reactive T cells against myelin antigens in the central nervous system (CNS). The model also addresses the modulation of proinflammatory neurotoxic responses by the generation of regulatory T cells (adaptive tolerance) and clarifies the role of innate tolerance, a part of the immune system that has been little explored in MS to date. Some ramifications of the model are mentioned, including its relevance to existing disease-modifying therapies and the need to look more closely at the innate immune system for future therapeutic targets. Drug Dev Res 72:674-688,

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Resistance to experimental autoimmune encephalomyelitis development in Lewis rats from a conventional animal facility

Abstract: Experimental autoimmune encephalomyelitis (EAE) is an inflammatory disease of the brain and spinal cord

Cited by 11 publications

References 32 publications

Ophthalmopathology in rats with MBP-induced experimental autoimmune encephalomyelitis

Ophthalmopathology in rats with MBP-induced experimental autoimmune encephalomyelitis

Early Life Exposure to Lipopolysaccharide Suppresses Experimental Autoimmune Encephalomyelitis by Promoting Tolerogenic Dendritic Cells and Regulatory T Cells

Innate origins of multiple sclerosis pathogenesis: Implications for computer‐assisted design of disease‐modifying therapies

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