• Title, Summary, Keyword: experimental autoimmune encephalomyelitis

Search Result 24, Processing Time 0.039 seconds

Expression and localization of phospho-IkB in the central nervous system during experimental autoimmune encephalomyelitis in Lewis rats (자가면역성 뇌척수염 랫드의 중추신경계에서의 인산화된 IkB의 발현양상)

  • Hwang, In Sun;Jee, Young Heun
    • Korean Journal of Veterinary Research
    • /
    • v.45 no.1
    • /
    • pp.7-15
    • /
    • 2005
  • To elucidate the roles of phospho-IkB expression in the development and progression of EAE, we investigated the expression of phospho-IkB in the central nervous system (CNS) of rats during experimental autoimmune encephalomyelitis (EAE) using immunohistochemistry and Western blot analysis. In Western blot analysis, the increased expression of phospho-IkB went parallel to severity of EAE. The expression of phospho-IkB increased significantly at the peak stage of EAE followed by gradual decrease. Immunohistochemical studies showed that the phospho-IkB immunoreactivity was mainly expressed in inflammatory cells (macrophages, T cells) and glial cells (astrocytes, microglial cells) at the peak stage of EAE and disappeared at the recovery stage. These findings suggest that the phosphorylation of IkB is closely associated with autoimmune inflammation in the CNS and plays an important role in the initiation and progression of EAE.

Appearance of osteoporosis in rat experimental autoimmune encephalomyelitis

  • Ahn, Meejung;Kang, Sohi;Park, Channam;Kim, Jeongtae;Jung, Kyungsook;Yang, Miyoung;Kim, Sung-Ho;Moon, Changjong;Shin, Taekyun
    • Korean Journal of Veterinary Research
    • /
    • v.56 no.2
    • /
    • pp.117-120
    • /
    • 2016
  • Experimental autoimmune encephalomyelitis (EAE) in Lewis rats is characterized by transient paralysis followed by recovery. To evaluate whether transient paralysis in EAE affects bone density, tibiae of EAE rats were morphologically investigated using micro-computed tomography and histology. The parameters of bone health were significantly reduced at the peak stage of EAE rats relative to those of controls (p < 0.05). The reduction of bone density was found to remain unchanged, even in the recovery stage. Collectively, the present data suggest that osteoporosis occurs in paralytic rats with monophasic EAE, possibly through the disuse of hindlimbs and/or autoimmune inflammation.

STAT mRNA kinetics in the central nervous system during autoimmune encephalomyelitis in lewis rats

  • Jee, Young-heun;Hwang, In-sun;Shin, Tae-kyun;Moon, Chang-jong;Lim, Yoon-kyu;Yeo, In-kyu;Son, Hwa-young
    • Korean Journal of Veterinary Research
    • /
    • v.44 no.2
    • /
    • pp.163-169
    • /
    • 2004
  • To elucidate the molecular mechanisms of autoimmune inflammation in the central nervous system, we examined the expression and localization of STAT1, STAT3, STAT4 and STAT6 molecules during experimental autoimmune encephalomyelitis (EAE) by competitive PCR. In the present study, we quantitated IL-4 and IL-12 p40 mRNA by competitive PCR in the CNS during EAE. IL-4 mRNA was found at early and peak stages. On the other hand, the IL-12 p40 mRNA level reached maximal levels at the peak stage and still found at the recovery stage of the disease. We examined the kinetics of STAT mRNA in the CNS during EAE and demonstrated that STAT1 and STAT4 mRNA reached a maximal level at the peak stage of EAE, whereas STAT3 mRNA level increased gradually to the recovery stage. STAT6 mRNA increased rapidly at the early stage followed by gradual decrease till the recovery stage. Taken together, these findings suggest that STAT4 which was probably activated by IL-12 plays a pro-inflammatory role and that STAT3 which was activated throughout the disease course seems to serve as a transducer of anti-inflammatory signals.

The expression of interleukin-1β converting enzyme in experimental autoimmune encephalomyelitis (자기면역성 뇌척수염에서 interleukin-1β converting enzyme의 발현)

  • Moon, Chang-jong;Kim, Seung-joon;Lee, Yong-duk;Shin, Tae-kyun
    • Korean Journal of Veterinary Research
    • /
    • v.39 no.3
    • /
    • pp.538-544
    • /
    • 1999
  • To elucidate the involvement of interleukin-$1{\beta}$ converting enzyme (ICE) in the course of experimental autoimmune encephalomyelitis (EAE), we induced EAE by immunizing rats with an emulsion of rat spinal cord homogenate with complete Freund's adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5mg/ml) and then examined the expression of ICE in the spinal cord of rats with EAE. In normal rat spinal cords, ICE is constitutively, but weakly, expressed in ependymal cells, neurons, and some neuroglial cells. In EAE, many inflammatory cells are positive for ICE, and the majority of ICE+ cells were identified as ED1+ macrophages. During this stage of EAE, the number of ICE+ cells in brain cells, including neurons and astrocytes, increased and these cells also had increased ICE immunoreactivity. These findings suggest that the upregulation of ICE in both brain cells and invading hematogenous cells is stimulated by a secretory product from inflammatory cells, and that this enzyme is involved in the pathogenesis of EAE via the production of IL-1 beta.

  • PDF

Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways

  • Lee, Min Jung;Chang, Byung Joon;Oh, Seikwan;Nah, Seung-Yeol;Cho, Ik-Hyun
    • Journal of Ginseng Research
    • /
    • v.42 no.4
    • /
    • pp.436-446
    • /
    • 2018
  • Background: The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. Methods: We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanism of KRGE on spinal myelination. Results: Pretreatment with KRGE (100 mg/kg, orally) for 10 days before immunization with myelin basic protein $(MBP)_{68-82}$ peptide exerted a protective effect against demyelination in the spinal cord, with inhibited recruitment and activation of immune cells including microglia, decreased mRNA expression of detrimental inflammatory mediators (interleukin-6, interferon-${\gamma}$, and cyclooxygenase-2), but increased mRNA expression of protective inflammatory mediators (insulin-like growth factor ${\beta}1$, transforming growth factor ${\beta}$, and vascular endothelial growth factor-1). These results were associated with significant downregulation of p38 mitogen-activated protein kinase and nuclear factor-${\kappa}B$ signaling pathways in microglia/macrophages, T cells, and astrocytes. Conclusion: Our findings suggest that KRGE alleviates spinal demyelination in acute experimental autoimmune encephalomyelitis through inhibiting the activation of the p38 mitogen-activated protein kinase/nuclear factor-${\kappa}B$ signaling pathway. Therefore, KRGE might be used as a new therapeutic for autoimmune disorders such as multiple sclerosis, although further investigation is needed.

A potential role of Schwann cells in spinal nerve roots in autoimmune central nervous system diseases

  • Moon, Changjong;Lee, Yongduk;Shin, Taekyun
    • Korean Journal of Veterinary Research
    • /
    • v.44 no.4
    • /
    • pp.483-486
    • /
    • 2004
  • The expression of nestin and vimentin in the spinal nerve roots of rats with experimental autoimmune encephalomyelitis (EAE) was studied to ascertain whether Schwann cells in the peripheral nerves respond to acute central nervous system autoimmune injury. Immunohistochemistry demonstrated that nestin was constitutively expressed in the dorsal roots of spinal nerves in control rats; its expression was enhanced in the spinal nerve roots of rats with EAE. Vimentin expression was weak in control rat spinal nerve roots, and it was increased in the dorsal roots of rats with EAE. It is postulated that normal animals have multipotent progenitor cells that constitutively express nestin and vimentin in the spinal nerve roots. In response to an injury of the central nervous system, these multipotent Schwann cells are activated in the spinal nerve roots through the expression of the intermediate filament proteins vimentin and nestin.

The Anti-Inflammatory Effects of Oral-Formulated Tacrolimus in Mice with Experimental Autoimmune Encephalomyelitis

  • Kim, Myung-Jin;Sung, Jung-Joon;Kim, Seung Hyun;Kim, Jeong-Min;Jeon, Gye Sun;Mun, Seog-Kyun;Ahn, Suk-Won
    • Journal of Korean Medical Science
    • /
    • v.32 no.9
    • /
    • pp.1502-1507
    • /
    • 2017
  • Multiple sclerosis (MS) is a T-lymphocyte-mediated autoimmune disease that is characterized by inflammation in the central nervous system (CNS). Although many disease-modifying therapies (DMTs) are presumed effective in patients with MS, studies on the efficacy and safety of DMTs for preventing MS relapse are limited. Therefore, we tested the immunosuppressive anti-inflammatory effects of oral-formulated tacrolimus (FK506) on MS in a mouse model of experimental autoimmune encephalomyelitis (EAE). The mice were randomly divided into 3 experimental groups: an untreated EAE group, a low-dose tacrolimus-treated EAE group, and a high-dose tacrolimus-treated EAE group. After autoimmunization of the EAE mice with myelin oligodendrocyte glycoprotein, symptom severity scores, immunohistochemistry of the myelination of the spinal cord, and western blotting were used to evaluate the EAE mice. After the autoimmunization, the symptom scores of each EAE group significantly differed at times. The group treated with the larger tacrolimus dose had the lowest symptom scores. The tacrolimus-treated EAE groups exhibited less demyelination and inflammation and weak immunoreactivity for all of the immunization biomarkers. Our results revealed that oral-formulated tacrolimus inhibited the autoimmunization in MS pathogenesis by inactivating inflammatory cells.

Amelioration of experimental autoimmune encephalomyelitis by Ishige okamurae

  • Ahn, Meejung;Kim, Jeongtae;Yang, Wonjun;Choi, Yuna;Ekanayake, Poornima;Ko, Hyunju;Jee, Youngheun;Shin, Taekyun
    • Anatomy and Cell Biology
    • /
    • v.51 no.4
    • /
    • pp.292-298
    • /
    • 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.

Expression of protein kinase C in the spinal cords of rats with autoimmune encephalomyelitis (뇌염모델에서 Protein Kinase C의 발현에 관한 연구)

  • Shin, Tae-Kyun;Kim, Hyung-Min;Tanuma, Naoyuki;Matsumoto, Yoh
    • Korean Journal of Veterinary Pathology
    • /
    • v.1 no.1
    • /
    • pp.26-32
    • /
    • 1997
  • Protein kinase C an enzyme of signal transduction has been known to regulate cell proliferation activation as well as apoptosis in some cancer cell lines. To explore the role of PKC in the course of cell mediated autoimmune disease such as experimental autoimmune encephalomyelitis (EAE) EAE was induced in Lewis rats(6-8 weeks old) with immunization of myelin basic protein supplemented with complete Freund's adjuvants and affected spinal cords were sampled at days 13 postimmunization(PI) as peak stage of EAE and at days 21 PI as recovery stage. The spinal cords with EAE were subjected to Northern blot analysis and insitu hybridization of PKC delta which is one of prominant isotypes of PKC in the haematopoietic cells. Northern blot analysis showed that levels of PKS delta mRNA in the spinal cords of rats withEAE was significantly increased at days 13 PI in which inflammatory cells including T cells and macrophages in the EAE lesions appeared. however the stage. By in situ hybridization signals of PKC delta in EAE lesions was intensely expressed on the delta is also expressed on some brain cells in normal rat central nervous system This finding suggests that PKC plays an important role on either activation of inflammatory cells including encephalitogenic T cells and macrophages or apoptotic elimination of some inflammatory cells depending on the stge of EAE.

  • PDF

Immunohistochemical study of CPP32 (Caspase-3) in the spinal cords of rats with experimental autoimmune encephalomyelitis (자기면역성 뇌척수염 조직에서 CPP32의 면역조직화학적 관찰)

  • Shin, Tae-kyun;Moon, Chang-jong;Ahn, Mee-jung;Wie, Myung-bok
    • Korean Journal of Veterinary Research
    • /
    • v.40 no.3
    • /
    • pp.431-437
    • /
    • 2000
  • The aim of this study was to evaluate the involvement of CPP32 (caspase-3), one of the death-related enzymes, in the course of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats immunized with an emulsion of rat spinal cord homogenate with complete Freunds adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5mg/ml). The expression of CPP32 in the spinal cords of rats with EAE was studied. In normal rat spinal cords, CPP32 is constitutively, but weakly, expressed in neurons and some neuroglial cells. In the EAE spinal cords, many inflammatory cells were positive for CPP 32, and the majority of CPP32(+) cells were identified as ED1(+) macrophages. During this stage of EAE, the number of CPP32(+) cells in brain cells, including neurons and astrocytes, increased, and these cells also had increased CPP32 immunoreactivity. CPP32 immunor eactivity was not always matched with apoptosis of inflammatory cells in EAE lesions. We speculate that CPP32, which is constitutlvely expressed in brain cells, increases in response to neuroimmunological stimulation in both brain neuronal cells and inflammatory cells. The functional role of CPP32 in neuroimmunological disorders is discussed.

  • PDF