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

• The Journal of Korean Medicine
• /
• v.40 no.4
• /
• pp.84-90
• /
• 2019

Objectives: Chronic fatigue syndrome (CFS) is a debilitating illness impairing seriously quality of life, while CFS would be an optimized target disorder of Korean medicine. This study aims to present the recent information especially in aspect of medical policy and new diagnosis criteria for CFS. Methods: The literature survey was conducted using the terms of "chronic fatigue syndrome", "myalgic encephalomyelitis" and "fibromyalgia" in PubMed database and Google database in its entirety from January 2011 to February 2019. The in-depth review was made focusing on the changes in policy and medical perspective for CFS. Results: Recently large medical attentions and researches for CFS have been existed worldwide. By supporting of USA government, IOM made a report which leaded to a turning point in clinical practices and research in 2015. This report recommended a new name of CFS to systemic exertion intolerance disease (SEID), and new diagnostic criteria focusing on post-exertional malaise, unrefreshing sleep, cognitive impairment and orthostatic intolerance. The medical perspective also was changed into "a serious, chronic, complex, systemic disease" from a psychological-like disorder, and then UAS and EU governments sharply increased the research grants. Conclusions: This study provided practitioners in Korean medicine (KM) a core information about the recent changes in CFS-related perspectives. This review would be helpful for KM-derived researches or therapeutics development for CFS.

• Korean Journal of Veterinary Service
• /
• v.34 no.1
• /
• pp.19-29
• /
• 2011

Prevalence of major legal communicable diseases in chickens and ducks, which had occurred in Jeonbuk province from year 2004 to 2008. Total 283 farms 1,419,244 chickens and ducks have been affected by avian diseases. Specifically, fowl typhoid (FT) occurred in 92 farms 416,600 chickens, Marek's disease (MD) in 45 farms 145,563, duck virus hepatitis (DVH) in 31 farms 199,200, infectious bursal disease (IBD) in 27 farms 113,220, infectious bronchitis (IB) in 27 farms 280,300, low pathogenic avian influenza (LPAI) in 26 farms 78,495, avian mycoplasmosis in 16 farms 103,774, Newcastle disease (ND) occurred in 11 farms 61,052, avian encephalomyelitis (AE) in 7 farms 21,000, Pullorum disease (PD) occurred in 1 farm 40. According to total analysis about major legal communicable diseases, 1 species of first-class legal communicable diseases have occurred, 3 species of second-class and 6 species of third-class all adding up to 10 species. In the first-class diseases, Newcastle disease have occurred. Pullorum and fowl typhoid, duck virus hepatitis in the second-class have occurred and as third-class diseases, Marek's disease, Infectious bursal disease, Infectious bronchitis, avian mycoplasmosis, avian encephalomyelitis, low pathogenic avian influenza have occurred.

• Clinical and Experimental Pediatrics
• /
• v.64 no.3
• /
• pp.103-110
• /
• 2021

Inflammatory or immune-mediated demyelinating central nervous system (CNS) syndromes include a broad spectrum of clinical phenotype and different overlapping diseases. Antibodies against myelin oligodendrocyte glycoprotein (MOG-Ab) have been found in some cases of these demyelinating diseases, particularly in children. MOG-Ab is associated with a wider clinical phenotype not limited to neuromyelitis optica spectrum disorder, with most patients presenting with optic neuritis, acute disseminated encephalomyelitis (ADEM) or ADEM-like encephalitis with brain demyelinating lesions, and/or myelitis. Using specific cell-based assays, MOG-Ab is becoming a potential biomarker of inflammatory demyelinating disorders of the CNS. A humoral immune reaction against MOG was recently found in monophasic diseases and recurrent/multiphasic clinical progression, particularly in pediatric patients. This review summarizes the data regarding MOG-Ab as an impending biological marker for discriminating between these diverse demyelinating CNS diseases and discusses recent developments, clinical applications, and findings regarding the immunopathogenesis of MOG-Ab-associated disorders.

• Biomolecules & Therapeutics
• /
• v.27 no.2
• /
• pp.152-159
• /
• 2019

Multiple sclerosis (MS) is an autoimmune disease characterized by progressive neuronal loss, neuroinflammation, axonal degeneration, and demyelination. Previous studies have reported that 6-shogaol, a major constituent of ginger (Zingiber officinale rhizome), and its biological metabolite, 6-paradol, have anti-inflammatory and anti-oxidative properties in the central nervous system (CNS). In the present study, we investigated whether 6-shogaol and 6-paradol could ameliorate against experimental autoimmune encephalomyelitis (EAE), a mouse model of MS elicited by myelin oligodendrocyte glycoprotein ($MOG_{35-55}$) peptide immunization with injection of pertussis toxin. Once-daily administration of 6-shogaol and 6-paradol (5 mg/kg/day, p.o.) to symptomatic EAE mice significantly alleviated clinical signs of the disease along with remyelination and reduced cell accumulation in the white matter of spinal cord. Administration of 6-shogaol and 6-paradol into EAE mice markedly reduced astrogliosis and microglial activation as key features of immune responses inside the CNS. Furthermore, administration of these two molecules significantly suppressed expression level of tumor necrosis $factor-{\alpha}$, a major proinflammatory cytokine, in EAE spinal cord. Collectively, these results demonstrate therapeutic efficacy of 6-shogaol or 6-paradol for EAE by reducing neuroinflammatory responses, further indicating the therapeutic potential of these two active ingredients of ginger for MS.

• Korean Journal of Veterinary Research
• /
• v.54 no.4
• /
• pp.209-218
• /
• 2014

Experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), reflects pathophysiologic steps in MS such as the influence of T cells and antibodies reactive to the myelin sheath, and the cytotoxic effect of cytokines. Galectin-9 (Gal-9) is a member of animal lectins that plays an essential role in various biological functions. The expression of Gal-9 is significantly enhanced in MS lesions; however, its role in autoimmune disease has not been fully elucidated. To identify the role of Gal-9 in EAE, we measured changes in mRNA and protein expression of Gal-9 as EAE progressed. Expression increased with disease progression, with a sharp rise occurring at its peak. Gal-9 immunoreactivity was mainly expressed in astrocytes and microglia of the central nervous system (CNS) and macrophages of spleen. Flow cytometric analysis revealed that $Gal-9^+CD11b^+$ cells were dramatically increased in the spleen at the peak of disease. Increased expression of tumor necrosis factor (TNF)-R1 and p-Jun N-terminal kinase (JNK) was observed in the CNS of EAE mice, suggesting that TNF-R1 and p-JNK might be key regulators contributing to the expression of Gal-9 during EAE. These results suggest that identification of the relationship between Gal-9 and EAE progression is critical for better understanding Gal-9 biology in autoimmune disease.

• Korean Journal of Veterinary Research
• /
• v.51 no.3
• /
• pp.217-225
• /
• 2011

Glatiramer acetate (GA; Copaxone) has been shown to be effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). It has been recently shown that GA-reactive T cells migrate through the blood-brain barrier, accumulate in the central nervous system (CNS), secrete antiinflammatory cytokines and suppress production of proinflammatory cytokines of EAE and MS. Development of EAE requires coordinated expression of a number of genes involved in the activation and effector functions of inflammatory cells. Activation of inflammatory cells is regulated at the transcriptional level by several families of transcription factors. One of these is the nuclear factor kappa B ($NF{\kappa}B$) family which is present in a variety of cell types and involved in the activation of immune-relative genes during inflammatory process. Since it is highly activated at site of inflammation, $NF{\kappa}B$ activation is also implicated in the pathogenesis of EAE. In this study, we examined whether the inhibition of $NF{\kappa}B$ activation induced by GA can have suppressive therapeutic effects in EAE mice. We observed the expression of $NF{\kappa}B$ and phospho-$I{\kappa}B$ proteins increased in GA-treated EAE mice compared to EAE control groups. The immunoreactivity in inflammatory cells and glial cells of $NF{\kappa}B$ and phospho-$I{\kappa}B$ significantly decreased at the GA-treated EAE mice. These results suggest that treatment of GA in EAE inhibits the activation of $NF{\kappa}B$ and phophorylation of $I{\kappa}B$ in the CNS. Subsequently, the inhibition of $NF{\kappa}B$ activation and $I{\kappa}B$ phosphorylation leads to the anti-inflammatory effects thereby to reduce the progression and severity of EAE.

• Korean Journal of Veterinary Research
• /
• v.33 no.2
• /
• pp.295-300
• /
• 1993

Central nervous system of two dogs with natural canine distemper was investigated histopathologically and immunocytochemically with antisera to MBP, MAG and GFAP. Histopathologically, there were neuronal degeneration and diffuse gliosis in the cerebrum, vacuolar degeneration, hypertrophy of astrocytes and demyelination in cerebellar white matter adjacent to the 4th ventricle and optic tracts showing non-inflammatory demyelinating encephalomyelitis (Summers and Appel, 1987). Immunohistochemically, there was a concurrent disappearance of MBP and MAG in the well developed demyelinating lesion in the cerebellar white matter. At the margin of demyelination, Loss of both MBP and MAG varied on the stage of demyelinating process. GFAP-positive astrocytes were hypertrophied and contained canine distemper virus intranuclear inclusions. GFAP-positive fibers were increased at the early stage of demyelination, and then were not immunoreaeted at the well developed demyelination. Hypertrophic astrocytes with intranuclear inclusions were commonly identified in the interfascular layer without myelin vacuolation and demyelination. This is the first study of primary demyelination and astroglial reactions in natural CDE investigated using immunocytochemistry of two myelin proteins and GFAP. Concurrent loss of MBP and MAG suggest that the myelin sheath is the target in the demyelinating process in CDE.

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

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