• Anatomy and Cell Biology
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• v.51 no.4
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• pp.292-298
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• 2018

Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune central nervous system disease characterized by inflammation with oxidative stress. The aim of this study was to evaluate an anti-inflammatory effect of Ishige okamurae on EAE-induced paralysis in rats. An ethanolic extract of I. okamurae significantly delayed the first onset and reduced the duration and severity of hind-limb paralysis. The neuropathological and immunohistochemical findings in the spinal cord were in agreement with these clinical results. T-cell proliferation assay revealed that the ethyl-acetate fraction of I. okamurae suppressed the proliferation of myelin basic protein reactive T cells from EAE affected rats. Flow cytometric analysis showed $TCR{\alpha}{\beta}^+$ T cells was significantly reduced in the spleen of EAE rats with I. okamurae treatment with concurrent decrease of inflammatory mediators including tumor necrosis $factor-{\alpha}$ and cyclooxygenase-2. Collectively, it is postulated that I. okamurae ameliorates EAE paralysis with suppression of T-cell proliferation as well as decrease of pro-inflammatory mediators as far as rat EAE is concerned.

• Korean Journal of Veterinary Research
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• v.51 no.2
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• pp.139-149
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• 2011

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory disease in the murine central nervous system (CNS) and has long been used as an animal model for human multiple sclerosis. Development of EAE requires coordinated expression of a number of genes that are involved in the activation and effector functions of inflammatory cells. Galectin-3 (Gal-3) is a member of the betagalactoside- binding lectin family and plays an important role in inflammatory responses through its functions on cell activation, cell migration or inhibition of apoptosis. We investigated the functional role of Gal-3 in EAE mice following immunization with myelin oligodendrocyte glycoprotein $(MOG)_{35-55}$ peptide. During the peak stage of EAE, the localization of Gal-3 in inflammatory cells markedly increased in subarachnoid membranes and perivascular regions of CNS. In contrast, Gal-3 was weakly detected in cerebrum and spinal of the recovery stage of EAE. Consistent with this finding, western blot analysis revealed that Gal-3 expression was significantly increased at the peak stage while it was slightly decreased at the recovery stage in the CNS. In addition, the population of $CD11b^{+}$ macrophage expressing Gal- 3 in spleen of EAE mice was markedly increased compared with control mice. In fact, most of activated macrophages isolated from spleen of EAE mice expressed Gal-3. Taken together, our results demonstrate that the over-expression of Gal-3 in activated macrophages may play a key role in promoting inflammatory cells in the CNS during EAE.

• Korean Journal of Veterinary Research
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• v.44 no.3
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• pp.349-355
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• 2004

The aim of this study was to evaluate the expression of galectin-3, one of beta-galactoside-binding proteins, in the experimental autoimmune encephalomyelitis(EAE) model of Lewis rats or non-obese diabetic (NOD) mice. Western blot analysis showed that galectin-3 was weakly expressed in the spinal cords of complete Freund's adjuvant(CFA) immunized control rats. In EAE, however, galectin-3 expression was significantly increased at the peak stage(days 14 post-immunization), while it was decreased slightly at the recovery stage(day 21 post-immunization). Immunohistochemical analysis showed that galectin-3 was detected in some macrophages in demyelinating lesions of NOD mice, while galectin-3 was immunoreacted in some inflammatory cells in the perivascular cuffing in rat EAE lesions. Collectively, it is postulated that the expression of galectin-3 is significantly increased in response to neuroimmunological stimulation in the central nervous system, whereas it is weak in normal rats and mice.

• Journal of Veterinary Science
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• v.25 no.3
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• pp.35.1-35.13
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• 2024

Importance: Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by inflammation within the central nervous system. However, inflammation in non-neuronal tissues, including the lungs, has not been fully evaluated. Objective: This study evaluated the inflammatory response in lungs of EAE mice by immunohistochemistry and histochemistry. Methods: Eight adult C57BL/6 mice were injected with myelin oligodendrocyte glycoprotein_35-55 to induce the EAE. Lungs and spinal cords were sampled from the experimental mice at the time of sacrifice and used for the western blotting, histochemistry, and immunohistochemistry. Results: Histopathological examination revealed inflammatory lesions in the lungs of EAE mice, characterized by infiltration of myeloperoxidase (MPO)- and galectin-3-positive cells, as determined by immunohistochemistry. Increased numbers of collagen fibers in the lungs of EAE mice were confirmed by histopathological analysis. Western blotting revealed significantly elevated level of osteopontin (OPN), cluster of differentiation 44 (CD44), MPO and galectin-3 in the lungs of EAE mice compared with normal controls (p < 0.05). Immunohistochemical analysis revealed both OPN and CD44 in ionized calcium-binding adapter molecule 1-positive macrophages within the lungs of EAE mice. Conclusions and Relevance: Taken together, these findings suggest that the increased OPN level in lungs of EAE mice led to inflammation; concurrent increases in proinflammatory factors (OPN and galectin-3) caused pulmonary impairment.

• Korean Journal of Veterinary Research
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• v.46 no.3
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• pp.177-184
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• 2006

Experimental autoimmune encephalomyelitis (EAE) is a disease model of multiple sclerosis (MS) that is characterized by remittance and relapse of the disease and autoimmune and demyelinating lesions in the central nervous system (CNS). Autoimmune inflammation is maintained by secretion of a large number of protein. Previous studies have suggested that transcripts encoding osteopontin (OPN) are frequently detected in the mRNA population of MS plaques. To elucidate the functional role of OPN in initiation and development of EAE, we examined the expression and localization of OPN in the spinal cord during acute EAE. We demonstrated that OPN significantly increased at the early stage of EAE and slightly declined thereafter by western blot analysis. An immunohistochemical study revealed that OPN was constitutively expressed in some glial cells (microglia, astrocytes) of white matter and neurons in the CNS of control rats. OPN expression was shown to be increased in the same cells at the early and peak stage of EAE. To identity cells expressing OPN by double-immunofluorescence labeling, we labeled rat spinal cord sections for OPN with a monoclonal OPN antibody and with mAbs for astrocyte (GFAP), microglia/macrophage (OX42)-specific markers. The major cell types of OPN-expressing cells were activated astrocytes and microglia in the adjacent inflammatory lesions. Interestingly, OPN was mainly expressed in the end feet of astrocytes around vascular cell adhesion molecule-1 (VCAM-1) expressing endothelial cells of CNS blood vessel. These findings suggest that increased levels of OPN in activated glial cell may play an important role in the recruitment of inflammatory cells into the CNS parenchyma during EAE.

• Annals of Clinical Neurophysiology
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• v.11 no.1
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• pp.33-36
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• 2009

Bickerstaff's brainstem encephalitis (BBE) is an autoimmune central nervous system disorder. It can occur in more limited forms and may overlap with Guillain-Barr$\acute{e}$ syndrome (GBS). A 49-year-old female presented with rapidly progressive paralytic ileus, urinary retention, deep drowsiness, ophthalmoplegia, dysarthria, ataxia, quadriparesis and hyporeflexia after viral meningitis. She was diagnosed as BBE with GBS and treated with immunoglobulin. She was completely recovered after 1 month. It is a rare case of BBE overlapping with GBS presenting with severe paralytic ileus.

• Childhood Kidney Diseases
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• v.8 no.1
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• pp.80-85
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• 2004

The systemic lupus erythematosus(SLE) is a systemic inflammatory disease caused by autoimmune mechanism, involving blood cells, the kidney, the central nervous system, and etc. The heart is one of the frequently involved organs but it is rare as an initial manifestation. Therefore, early suspicion and accurate diagnosis followed by aggressive immunosuppressive therapy including corticosteroid is mandatory for heart-involved patients. We experienced a case of pericardial effusion as an initial manifestation of childhood SLE, which showed immediate response to corticosteroid.

• Journal of Genetic Medicine
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• v.19 no.2
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• pp.57-62
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• 2022

Systemic autoinflammatory diseases (SAIDs) are characterized by unprovoked inflammatory episodes such as recurrent/periodic fever, serositis, skin lesions, abdominal symptoms, arthritis/arthralgia, and central nervous system involvement. Genetic diagnosis of SAIDs has been challenging because disease manifestations overlap among themselves and with other immunological disease categories, such as infection and autoimmune diseases. However, the advent of next-generation sequencing (NGS) technologies and expanding knowledge about the innate immunity and inflammation have made the routine genetic diagnosis of SAIDs possible. Here, we review the recurrent/periodic fevers, other recently identified autoinflammatory diseases, and type I interferonopathies, and discuss the clinical usefulness of NGS targeted sequencing for SAIDs, and recent advance of understandings for this heterogeneous disease group as for underlying primary immunodeficiency.

• Annals of Clinical Neurophysiology
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• v.25 no.1
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• pp.19-26
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• 2023

Autonomic dysfunction occurs frequently in multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Patients with either condition may present with autonomic symptoms such as bladder, sexual, cardiovascular, thermoregulatory, and gastrointestinal dysfunction, and fatigue, but autonomic symptoms that affect quality of life are underrecognized in clinical practice. The immunopathogenesis of MS has been considered to be associated with autonomic dysfunction. Applying appropriate treatment strategies for autonomic dysfunction is important to improve the quality of life of patients. Here we review autonomic dysfunction and how this is managed in patients with MS and NMOSD.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.7
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• pp.565-568
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• 2017

Sjogren's syndrome is an autoimmune disease characterized by dry mouth and neutropenia. Although it does not commonly involve the central nervous system, Sjogren's syndrome sometimes affects small vessels through microangiopathic alterations. A 34-year-old woman was hospitalized for left upper quadrantanopia and a tingling sensation in the left hemibody. Brain magnetic resonance imaging revealed acute infarction in the right posterior cerebral artery territory. In laboratory tests, antinuclear (FANA2+) and anti-DNA antibodies (anti-SS-A (Ro)) were detected. Salivary gland scintigraphy revealed moderately decreasedexcretion of saliva. Based on these findings, we concluded she had Sjogren's syndrome. As in this patient, large vessel involvement in Sjogren's syndrome is far less common. Furthermore, it is difficult to administer antiplatelet drugsto patients with thrombocytopenia in Sjogren's syndrome. This is a case of the patient with Sjogren's syndrome that involved thrombocytopenia and large vessel invasion who was treated with antiplatelet drugs and hydroxychloroquine.