Nitric oxide localized to spinal cords of mice with experimental allergic encephalomyelitis: an electron paramagnetic resonance study.

Lin, Robin F.; Lin, Tien‐Sung; Tilton, Ronald G.; Cross, Anne H.

doi:10.1084/jem.178.2.643

Cited by 144 publications

(47 citation statements)

References 35 publications

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“…Antioxidant treatment in experimental models of MS Activated macrophages and microglia may produce high levels of NO and H 2 O 2 that are involved in the pathogenesis of EAE (Lin et al, 1993;Ruuls et al, 1995;Minghetti & Levi, 1998). Treatment of EAE with catalase, a H 2 O 2 scavenger, markedly suppressed disease severity (Ruuls et al, 1995).…”

Section: Oxidative Stress and Antioxidantsmentioning

confidence: 99%

“…Reactive oxygen species (ROS) are implicated as mediators of demyelination and axonal damage in both MS and experimental allergic encephalomyelitis (EAE) (Lin et al, 1993;Cross et al, 1997;van der Goes et al, 1998), an animal model of MS. Local ROS levels increase dramatically under inflammatory conditions and exhaust the antioxidant defence potential within the lesions (Smith et al, 1999). These excessive ROS levels are primarily generated by activated macrophages and microglia (Fisher et al, 1988;Hartung et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Antioxidants and polyunsaturated fatty acids in multiple sclerosis

Meeteren¹,

Teunissen

Dijkstra

et al. 2005

Eur J Clin Nutr

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Section: Oxidative Stress and Antioxidantsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antioxidants and polyunsaturated fatty acids in multiple sclerosis

Meeteren¹,

Teunissen

Dijkstra

et al. 2005

Eur J Clin Nutr

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“…For instance, administration of uric acid (UA), a natural inhibitor of select chemical reactions associated with ONOO Ϫ , to animals with EAE protects the blood-CNS barrier from permeability changes normally associated with the disease (30). As the production of the ONOO Ϫ precursor NO • is a hallmark of the CNS inflammatory response in both EAE (15,22) and acute Borna disease (15), we postulate that ONOO Ϫ may have a physiological role in neuroimmune responses to enhance BBB permeability and promote cell invasion into the CNS. To investigate whether this may be the case for a neurotropic virus infection, we have assessed the effects of UA treatment on BBB permeability, CNS inflammation, and clinical disease in immunocompetent adult rats acutely infected with BDV.…”

mentioning

confidence: 99%

“…Studies of experimental allergic encephalomyelitis (EAE) have provided considerable information concerning CNS inflammatory disease in the absence of an underlying viral infection. In this model, acute neurological disease is triggered by sensitization of CD4 T cells with myelin Ags, and CNS pathology has been associated with free radical production by inflammatory cells (21)(22)(23). Peroxynitrite (ONOO Ϫ ), the product of NO ⅐ and O 2 ⅐Ϫ , is believed to be an important toxic molecule in this context (24 -27).…”

mentioning

confidence: 99%

The Central Nervous System Inflammatory Response to Neurotropic Virus Infection Is Peroxynitrite Dependent

Hooper

Kean

Scott

et al. 2001

The Journal of Immunology

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We have recently demonstrated that increased blood-CNS barrier permeability and CNS inflammation in a conventional mouse model of experimental allergic encephalomyelitis are dependent upon the production of peroxynitrite (ONOO−), a product of the free radicals NO· and superoxide (O2·−). To determine whether this is a reflection of the physiological contribution of ONOO− to an immune response against a neurotropic pathogen, we have assessed the effects on adult rats acutely infected with Borna disease virus (BDV) of administration of uric acid (UA), an inhibitor of select chemical reactions associated with ONOO−. The pathogenesis of acute Borna disease in immunocompetent adult rats results from the immune response to the neurotropic BDV, rather than the direct effects of BDV infection of neurons. An important stage in the BDV-specific neuroimmune response is the invasion of inflammatory cells into the CNS. UA treatment inhibited the onset of clinical disease, and prevented the elevated blood-brain barrier permeability as well as CNS inflammation seen in control-treated BDV-infected rats. The replication and spread of BDV in the CNS were unchanged by the administration of UA, and only minimal effects on the immune response to BDV Ags were observed. These results indicate that the CNS inflammatory response to neurotropic virus infection is likely to be dependent upon the activity of ONOO− or its products on the blood-brain barrier.

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“…The presence of iNOS mRNA has been shown in experimental neurological inflammation [12], in the pancreas in experimental diabetes mellitus [ 13] and in experimental arthritis [14]. The production of NO itself in vivo has been shown by the use of electron paramagnetic resonance spectroscopy in allograft rejection [15], septic shock [16] and in experimental allergic encephalomyelitis [17].…”

Section: Introductionmentioning

confidence: 99%

Expression of the gene for inducible nitric oxide synthase in experimental glomerulonephritis in the rat

Cook

Ebrahim

Jansen

et al. 1994

Clinical and Experimental Immunology

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SUMMARYNitrite, a stable product of nitric oxide (NO), is synthesized in vitro by glomeruli in experimental glomerulonephritis. We have now studied the expression of the gene for inducible NO synthase (iNOS) in accelerated nephrotoxic nephritis (NTN). The purpose of the study was to confirm in vivo induction of iNOS in this model of immune complex disease, and to relate the onset of induction and the level of expression to pathogenic events in the model. Glomeruli from rats with NTN were isolated at 6h, 24h and 2, 4 and 7 days and total RNA extracted. RNA (10/ig) was reverse transcribed and polymerase chain reaction (PCR) was performed with primers homologous to rat vascular smooth muscle iNOS and rat 8 actin. A 222-base PCR product corresponding to iNOS mRNA was present in all experimental animals. iNOS expression was also found in activated macrophages, neutrophils and IL-1-stimulated but not unstimulated mesangial cells. Quantitative competitive PCR was carried out on glomerular samples using a 514-bp mutant ofa 735-bp PCR product. iNOS expression was present at low levels in normal glomeruli and was markedly enhanced at 6 h after the induction of glomerulonephrilis and peaked at 24 h. Increased iNOS expression persisted to day 7. 0 actin mRNA levels were similar in all glomerular specimens. This study demonstrates that there is in vivo induction of iNOS in immune complex glomerulonephritis, corresponding to the generation of nitrite we have previously reported. iNOS gene expression is detectable within 6h of induction of NTN, indicating the onset of gene transcription is closely related lo the inilial formation of immune complexes.

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Nitric oxide localized to spinal cords of mice with experimental allergic encephalomyelitis: an electron paramagnetic resonance study.

Cited by 144 publications

References 35 publications

Antioxidants and polyunsaturated fatty acids in multiple sclerosis

Antioxidants and polyunsaturated fatty acids in multiple sclerosis

The Central Nervous System Inflammatory Response to Neurotropic Virus Infection Is Peroxynitrite Dependent

Expression of the gene for inducible nitric oxide synthase in experimental glomerulonephritis in the rat

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