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Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Oxidative Injury and Iron Redistribution Are Pathological Hallmarks of Marmoset Experimental Autoimmune
Jordon Dunham1, Jan Bauer1, Graham R Campbell1
1From the Department of Immunobiology, Biomedical Primate Research Centre, Rijswijk, The Netherlands (JD, NvD, BAH, YSK); Department of Neuroscience, University Medical Center, University of Groningen, Groningen, The Netherlands (JD, BAH, JDL); Medical University of Vienna, Center for Brain Research, Vienna, Austria (JB, HL); Centre for Neuroregeneration, University of Edinburgh, Edinburgh, United Kingdom (GRC, DJM); and Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands (SMAvdP, JvH).
Abstract:
Oxidative damage and iron redistribution are associated with the pathogenesis and progression of multiple sclerosis (MS), but these aspects are not entirely replicated in rodent experimental autoimmune encephalomyelitis (EAE) models. Here, we report that oxidative burst and injury as well as redistribution of iron are hallmarks of the MS-like pathology in the EAE model in the common marmoset. Active lesions in the marmoset EAE brain display increased expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (p22phox, p47phox, and gp91phox) and inducible nitric oxide synthase immunoreactivity within lesions with active inflammation and demyelination, coinciding with enhanced expression of mitochondrial heat-shock protein 70 and superoxide dismutase 1 and 2. The EAE lesion-associated liberation of iron (due to loss of iron-containing myelin) was associated with altered expression of the iron metabolic markers FtH1, lactoferrin, hephaestin, and ceruloplasmin. The enhanced expression of oxidative damage markers in inflammatory lesions indicates that the enhanced antioxidant enzyme expression could not counteract reactive oxygen and nitrogen species-induced cellular damage, as is also observed in MS brains. This study demonstrates that oxidative injury and aberrant iron distribution are prominent pathological hallmarks of marmoset EAE thus making this model suitable for therapeutic intervention studies aimed at reducing oxidative stress and associated iron dysmetabolism.
Insights
Oxidative damage and iron redistribution are key features of multiple sclerosis-like pathology in marmoset EAE models. This finding highlights the marmoset EAE model
Area of Science:
- Neuroimmunology
- Neuroinflammation
- Pathology
Background:
- Oxidative damage and iron redistribution are implicated in multiple sclerosis (MS) pathogenesis.
- Existing rodent experimental autoimmune encephalomyelitis (EAE) models do not fully replicate these MS pathological features.
- A need exists for better animal models to study MS pathology and test therapies.
Purpose of the Study:
- To investigate oxidative burst, iron redistribution, and associated molecular changes in the common marmoset EAE model.
- To determine if the marmoset EAE model accurately reflects MS-like pathology concerning oxidative stress and iron metabolism.
- To assess the suitability of the marmoset EAE model for therapeutic intervention studies targeting oxidative stress and iron dysmetabolism.
Main Methods:
- Induction of EAE in common marmosets.
- Immunohistochemical analysis of inflammatory lesions in the marmoset brain.
- Assessment of oxidative damage markers, antioxidant enzymes, and iron metabolic markers within lesions.
Main Results:
- Active lesions in marmoset EAE brains showed increased expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components (p22phox, p47phox, gp91phox) and inducible nitric oxide synthase.
- Enhanced expression of mitochondrial heat-shock protein 70 and superoxide dismutase 1 and 2 was observed in inflammatory lesions.
- Iron liberation in EAE lesions correlated with altered expression of iron metabolic markers (FtH1, lactoferrin, hephaestin, ceruloplasmin), indicating iron dysmetabolism.
Conclusions:
- Oxidative injury and aberrant iron distribution are prominent pathological hallmarks in the common marmoset EAE model.
- The marmoset EAE model effectively replicates key oxidative and iron-related pathological features of human MS.
- This model is suitable for evaluating therapeutic strategies aimed at mitigating oxidative stress and iron dysmetabolism in MS.
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