Base de dados : MEDLINE
Pesquisa : C10.114.703.700 [Categoria DeCS]
Referências encontradas : 553 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 56 ir para página                         

  1 / 553 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28734788
[Au] Autor:Taha O; Opitz T; Mueller M; Pitsch J; Becker A; Evert BO; Beck H; Jeub M
[Ad] Endereço:Department of Neurology, University of Bonn Medical Center, Sigmund Freud Straße 25, 53105 Bonn, Germany; Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Straße 25, 53105 Bonn, Germany.
[Ti] Título:Neuropathic pain in experimental autoimmune neuritis is associated with altered electrophysiological properties of nociceptive DRG neurons.
[So] Source:Exp Neurol;297:25-35, 2017 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy characterized by rapidly progressive paresis and sensory disturbances. Moderate to severe and often intractable neuropathic pain is a common symptom of GBS, but its underlying mechanisms are unknown. Pathology of GBS is classically attributed to demyelination of large, myelinated peripheral fibers. However, there is increasing evidence that neuropathic pain in GBS is associated with impaired function of small, unmyelinated, nociceptive fibers. We therefore examined the functional properties of small DRG neurons, the somata of nociceptive fibers, in a rat model of GBS (experimental autoimmune neuritis=EAN). EAN rats developed behavioral signs of neuropathic pain. This was accompanied by a significant shortening of action potentials due to a more rapid repolarization and an increase in repetitive firing in a subgroup of capsaicin-responsive DRG neurons. Na current measurements revealed a significant increase of the fast TTX-sensitive current and a reduction of the persistent TTX-sensitive current component. These changes of Na currents may account for the significant decrease in AP duration leading to an overall increase in excitability and are therefore possibly directly linked to pathological pain behavior. Thus, like in other animal models of neuropathic and inflammatory pain, Na channels seem to be crucially involved in the pathology of GBS and may constitute promising targets for pain modulating pharmaceuticals.
[Mh] Termos MeSH primário: Gânglios Espinais/fisiopatologia
Neuralgia/fisiopatologia
Neurite Autoimune Experimental/fisiopatologia
Nociceptores/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Fenômenos Eletrofisiológicos/fisiologia
Gânglios Espinais/patologia
Masculino
Neuralgia/patologia
Neurite Autoimune Experimental/patologia
Nociceptores/patologia
Medição da Dor/métodos
Ratos
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE


  2 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28601289
[Au] Autor:Pitarokoili K; Kohle F; Motte J; Fatoba O; Pedreiturria X; Gold R; Yoon MS
[Ad] Endereço:Department of Neurology, St. Josef Hospital, Ruhr-University of Bochum, Germany. Electronic address: kalliopi.pitarokoili@ruhr-uni-bochum.de.
[Ti] Título:Anti-inflammatory and immunomodulatory potential of human immunoglobulin applied intrathecally in Lewis rat experimental autoimmune neuritis.
[So] Source:J Neuroimmunol;309:58-67, 2017 Aug 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Intravenous human immunoglobulins dominate in the treatment of autoimmune neuropathies. We introduce intrathecal application as a new option for experimental autoimmune neuritis in Lewis rats. After immunisation with neuritogenic P2 peptide, we show a therapeutic and preventive effect of intrathecal human immunoglobulins (5-40mg/kg) on clinical and electrophysiological neuritis signs. Histology corroborated a lower degree of inflammation, demyelination, ICAM-1-dependent blood-nerve-barrier permeability and complement activation in the sciatic nerve. After preventive application, immunoglobulins induced a Th2 cytokine shift in the peripheral nerves already before clinical neuritis signs. Intrathecal immunoglobulin application could be a novel immunomodulatory option for autoimmune neuropathies.
[Mh] Termos MeSH primário: Anti-Inflamatórios/administração & dosagem
Imunoglobulinas/administração & dosagem
Fatores Imunológicos/administração & dosagem
Neurite Autoimune Experimental/tratamento farmacológico
Neurite Autoimune Experimental/patologia
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Injeções Espinhais
Neurite Autoimune Experimental/imunologia
Distribuição Aleatória
Ratos
Ratos Endogâmicos Lew
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Immunoglobulins); 0 (Immunologic Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170612
[St] Status:MEDLINE


  3 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28284349
[Au] Autor:Moriguchi K; Miyamoto K; Kusunoki S
[Ad] Endereço:Division of Neurology, Department of Internal Medicine 3, National Defense Medical College, Tokorozawa, Japan; Department of Internal Medicine, Japan Self Defense Forces Hanshin Hospital, Kawanishi, Japan.
[Ti] Título:4-Aminopyridine ameliorates experimental autoimmune neuritis in Lewis rats.
[So] Source:J Neuroimmunol;305:72-74, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We investigated the effect of 4-aminopyridine (4-AP) on experimental autoimmune neuritis (EAN) using a 4-AP-treated group in which 4-AP was administered in the diet, and a control group (n=10 per group). Electrophysiological and pathological assessment was performed in the sciatic nerve. The EAN clinical scores were significantly lower in the 4-AP-treated group than in the control group (p<0.05). The motor conductance velocity two weeks post-immunization was significantly higher in the 4-AP-treated group (p<0.05). Finally, 4-AP did not lead to pathological changes. Thus, 4-AP might be a potential therapeutic agent in demyelinating neuropathy.
[Mh] Termos MeSH primário: 4-Aminopiridina/uso terapêutico
Neurite Autoimune Experimental/tratamento farmacológico
Bloqueadores dos Canais de Potássio/uso terapêutico
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Animais
Modelos Animais de Doenças
Eletromiografia
Potencial Evocado Motor/efeitos dos fármacos
Potencial Evocado Motor/fisiologia
Adjuvante de Freund/toxicidade
Masculino
Proteínas da Mielina/toxicidade
Condução Nervosa/efeitos dos fármacos
Neurite Autoimune Experimental/induzido quimicamente
Neurite Autoimune Experimental/imunologia
Bloqueadores dos Canais de Potássio/farmacologia
Ratos
Ratos Endogâmicos Lew
Estatísticas não Paramétricas
Vacinação/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myelin Proteins); 0 (P2 peptide); 0 (Potassium Channel Blockers); 9007-81-2 (Freund's Adjuvant); BH3B64OKL9 (4-Aminopyridine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


  4 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28284336
[Au] Autor:Zhang M; Liu RT; Zhang P; Zhang N; Yang CL; Yue LT; Li XL; Liu Y; Li H; Du J; Duan RS
[Ad] Endereço:Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
[Ti] Título:Parthenolide inhibits the initiation of experimental autoimmune neuritis.
[So] Source:J Neuroimmunol;305:154-161, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A growing body of evidence suggests the anti-inflammatory and antitumor effects of parthenolide (PAR). Here we show that PAR treatment inhibits the initiation of experimental autoimmune neuritis (EAN), suppresses the production of TNF-α, IFN-γ, IL-1ß and IL-17, and decreases Th1 and Th17 cells at early time point. However, such anti-inflammatory effect vanishes later and PAR impedes the recovery of EAN in late phase, which is accompanied with inhibited apoptosis of inflammatory cells. Our results indicate that PAR plays dual roles in EAN and it is not proper to be applied in autoimmune diseases of nervous system.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Neurite Autoimune Experimental/tratamento farmacológico
Sesquiterpenos/uso terapêutico
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Anexina A5/metabolismo
Apoptose/fisiologia
Linfócitos T CD4-Positivos/patologia
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/fisiologia
Citocinas/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Citometria de Fluxo
Proteína Forkhead Box O3/metabolismo
Adjuvante de Freund/toxicidade
Linfonodos/patologia
Mycobacterium tuberculosis
Neurite Autoimune Experimental/etiologia
Ratos
Ratos Endogâmicos Lew
Nervo Isquiático/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Forkhead Box Protein O3); 0 (Sesquiterpenes); 2RDB26I5ZB (parthenolide); 9007-81-2 (Freund's Adjuvant)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


  5 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28260057
[Au] Autor:Zhou X; Wang Y; Wang Y; Cipriano P; Xiao B; Zhou W
[Ad] Endereço:Department of Neurology, Xiangya Hospital, Central­South University, Changsha, Hunan 410008, P.R. China.
[Ti] Título:Inhibition of triggering receptor expressed on myeloid cells-1 ameliorates experimental autoimmune neuritis.
[So] Source:Mol Med Rep;15(4):1565-1570, 2017 Apr.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Experimental autoimmune neuritis (EAN) is a cluster of differentiation 4+ T helper 1 cell-mediated inflammatory demyelinating disease of the peripheral nervous system and serves as a useful animal model for Guillain­Barré syndrome. Triggering receptor expressed on myeloid cells­1 (TREM­1) is an important receptor involved in sepsis and the innate inflammatory response. Linear plasmid 17 (LP 17) peptide is a competitive antagonist of TREM­1. To investigate the role of TREM­1 in EAN, 64 male Lewis rats were randomly divided into four groups: Normal saline, complete Freund's adjuvant, EAN and LP 17. The present study assessed the mRNA expression levels of TREM­1, tumor necrosis factor­α and interleukin­1ß in sciatic nerves and peripheral blood mononuclear cells. The results demonstrated that inhibiting TREM-1 by administering LP 17 ameliorated symptoms and reduced inflammation in EAN rats. The present study concluded that TREM­1 may be involved in the pathogenesis of EAN, and that inhibition of TREM-1 may ameliorate EAN.
[Mh] Termos MeSH primário: Neurite Autoimune Experimental/metabolismo
Neurite Autoimune Experimental/patologia
Receptores Imunológicos/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Masculino
Neurite Autoimune Experimental/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos Endogâmicos Lew
Receptores Imunológicos/metabolismo
Nervo Isquiático/patologia
Coloração e Rotulagem
Receptor Gatilho 1 Expresso em Células Mieloides
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (RNA, Messenger); 0 (Receptors, Immunologic); 0 (TREM1 protein, rat); 0 (Triggering Receptor Expressed on Myeloid Cells-1); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6167


  6 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28096232
[Au] Autor:Liu H; Wan C; Ding Y; Han R; He Y; Xiao J; Hao J
[Ad] Endereço:Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
[Ti] Título:PR-957, a selective inhibitor of immunoproteasome subunit low-MW polypeptide 7, attenuates experimental autoimmune neuritis by suppressing T 17-cell differentiation and regulating cytokine production.
[So] Source:FASEB J;31(4):1756-1766, 2017 Apr.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Experimental autoimmune neuritis (EAN) is a CD4 T-cell-mediated autoimmune inflammatory demyelinating disease of the peripheral nervous system. It has been replicated in an animal model of human inflammatory demyelinating polyradiculoneuropathy, Guillain-Barré syndrome. In this study, we evaluated the therapeutic efficacy of a selective inhibitor of the immunoproteasome subunit, low-MW polypeptide 7 (PR-957) in rats with EAN. Our results showed that PR-957 significantly delayed onset day, reduced severity and shortened duration of EAN, and alleviated demyelination and inflammatory infiltration in sciatic nerves. In addition to significantly regulating expression of the cytokine profile, PR-957 treatment down-regulated the proportion of proinflammatory T-helper (T )17 cells in sciatic nerves and spleens of rats with EAN. Data presented show the role of PR-957 in the signal transducer and activator of transcription 3 (STAT3) pathway. PR-957 not only decreased expression of IL-6 and IL-23 but also led to down-regulation of STAT3 phosphorylation in CD4 T cells. Regulation of the STAT3 pathway led to a reduction in retinoid-related orphan nuclear receptor γ t and IL-17 production. Furthermore, reduction of STAT3 phosphorylation may have directly suppressed T 17-cell differentiation. Therefore, our study demonstrates that PR-957 could potently alleviate inflammation in rats with EAN and that it may be a likely candidate for treating Guillain-Barré syndrome.-Liu, H., Wan, C., Ding, Y., Han, R., He, Y., Xiao, J., Hao, J. PR-957, a selective inhibitor of immunoproteasome subunit low-MW polypeptide 7, attenuates experimental autoimmune neuritis by suppressing T 17-cell differentiation and regulating cytokine production.
[Mh] Termos MeSH primário: Diferenciação Celular
Interleucinas/metabolismo
Neurite Autoimune Experimental/tratamento farmacológico
Oligopeptídeos/uso terapêutico
Inibidores de Proteassoma/uso terapêutico
Células Th17/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Interleucinas/genética
Masculino
Oligopeptídeos/farmacologia
Receptores Nucleares Órfãos/genética
Receptores Nucleares Órfãos/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Inibidores de Proteassoma/farmacologia
Ratos
Ratos Endogâmicos Lew
Fator de Transcrição STAT3/metabolismo
Células Th17/citologia
Células Th17/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukins); 0 (Oligopeptides); 0 (Orphan Nuclear Receptors); 0 (PR-957); 0 (Proteasome Inhibitors); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); EC 3.4.25.1 (LMP7 protein); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601147R


  7 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28082327
[Au] Autor:Gonsalvez DG; De Silva M; Wood RJ; Giuffrida L; Kilpatrick TJ; Murray SS; Xiao J
[Ad] Endereço:Department of Anatomy and Neuroscience, School of Biomedical Sciences, The University of Melbourne, Parkville, Victoria, Australia.
[Ti] Título:A Functional and Neuropathological Testing Paradigm Reveals New Disability-Based Parameters and Histological Features for P0180-190-Induced Experimental Autoimmune Neuritis in C57BL/6 Mice.
[So] Source:J Neuropathol Exp Neurol;76(2):89-100, 2017 02 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We assessed novel disability-based parameters and neuropathological features of the P0180-190 peptide-induced model of experimental autoimmune neuritis (EAN) in C57BL/6 mice. We show that functional assessments such as running capacity provide a more sensitive method for detecting alterations in disease severity than a classical clinical scoring paradigm. We performed detailed ultrastructural analysis and show for the first time that tomaculous neuropathy is a neuropathological feature of this disease model. In addition, we demonstrate that ultrastructural assessments of myelin pathology are sufficiently sensitive to detect significant differences in both mean G-ratio and mean axon diameter between mice with EAN induced with different doses of pertussis toxin. In summary, we have established a comprehensive assessment paradigm for discriminating variations in disease severity and the extent of myelin pathology in this model. Our findings indicate that this model is a powerful tool to study the pathogenesis of human peripheral demyelinating neuropathies and that this assessment paradigm could be used to determine the efficacy of potential therapies that aim to promote myelin repair and protect against nerve damage in autoimmune neuritides.
[Mh] Termos MeSH primário: Marcha/fisiologia
Neurite Autoimune Experimental/patologia
Neurite Autoimune Experimental/fisiopatologia
Fragmentos de Peptídeos/toxicidade
Recuperação de Função Fisiológica/fisiologia
Corrida/fisiologia
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neurite Autoimune Experimental/induzido quimicamente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Fragments)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlw110


  8 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27861905
[Au] Autor:Langert KA; Goshu B; Stubbs EB
[Ad] Endereço:Research Service, Department of Veterans Affairs, Edward Hines Jr. VA Hospital, Hines, Illinois, USA.
[Ti] Título:Attenuation of experimental autoimmune neuritis with locally administered lovastatin-encapsulating poly(lactic-co-glycolic) acid nanoparticles.
[So] Source:J Neurochem;140(2):334-346, 2017 Jan.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acute inflammatory demyelinating polyneuropathy (AIDP) is an aggressive antibody- and T-cell-mediated variant of Guillain-Barré Syndrome (GBS), a prominent and debilitating autoimmune disorder of the peripheral nervous system. Despite advancements in clinical management, treatment of patients with AIDP/GBS and its chronic variant CIDP remains palliative and relies on the use of non-specific immunemodulating therapies. Our laboratory has previously reported that therapeutic administration of statins safely attenuates the clinical severity of experimental autoimmune neuritis (EAN), a well-characterized animal model of AIDP/GBS, by restricting the migration of autoreactive leukocytes across peripheral nerve microvascular endoneurial endothelial cells that form the blood-nerve barrier. Despite these advancements, the clinical application of systemically administered statins for the management of inflammatory disorders remains controversial as a result of disappointingly inconclusive phase trials. Here, poly(lactic-co-glycolic) acid (PLGA) nanoparticles were evaluated as an alternative strategy by which to locally administer statins for the management of EAN. When tested in vitro, lovastatin-encapsulating PLGA nanoparticles elicited a marked increase in RhoB mRNA content in peripheral nerve microvascular endoneurial endothelial cells, similar to cells treated with activated unencapsulated lovastatin. Unilateral peri-neural administration of lovastatin-encapsulating PLGA nanoparticles, but not empty nanoparticles, to naïve Lewis rats similarly enhanced RhoB mRNA content in adjacent nerve and muscle tissue. When administered in this manner, serum levels of lovastatin were below the level of detection. Bilateral peri-neural administration of lovastatin-encapsulating PLGA nanoparticles to EAN-induced Lewis rats significantly attenuated EAN clinical severity while protecting against EAN-induced peripheral nerve morphological and functional deficits. This study provides the first proof-of-concept approach for the application of a nanoparticle-based local drug delivery platform for the management of inflammatory demyelinating diseases, including AIDP/GBS.
[Mh] Termos MeSH primário: Síndrome de Guillain-Barré/tratamento farmacológico
Lovastatina/farmacologia
Nanopartículas/administração & dosagem
Neurite Autoimune Experimental/tratamento farmacológico
Linfócitos T/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Cápsulas
Modelos Animais de Doenças
Glicóis/metabolismo
Ácido Láctico
Ácido Poliglicólico
Ratos
Nervo Isquiático/efeitos dos fármacos
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Capsules); 0 (Glycols); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); 9LHU78OQFD (Lovastatin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.13892


  9 / 553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27842213
[Au] Autor:Brunn A; Mihelcic M; Carstov M; Feind L; Wieser EC; Schmidt J; Utermöhlen O; Deckert M
[Ad] Endereço:Department of Neuropathology, University Hospital of Cologne, Cologne, Germany. Electronic address: anna.brunn@uk-koeln.de.
[Ti] Título:Toll-Like Receptor 2, Toll-Like Receptor 4, Myeloid Differentiation Response Gene 88, and Toll-IL-1 Receptor Domain-Containing Adaptor-Inducing Interferon-γ (TRIF) Selectively Regulate Susceptibility of P0 -Induced Murine Experimental Autoimmune Neuritis.
[So] Source:Am J Pathol;187(1):42-54, 2017 Jan.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The functional relevance of the innate immune system has not yet been dissected in P0 -induced murine experimental autoimmune neuritis. Therefore, the role of Toll-like receptor (TLR) 2, TLR4, myeloid differentiation response gene 88, and Toll-IL-1 receptor domain-containing adaptor-inducing interferon-γ (TRIF), factors critically involved in the TLR signaling pathway, was studied in experimental autoimmune neuritis. In the absence of TLR2, TLR4, myeloid differentiation response gene 88, or TRIF, the clinical course was significantly attenuated compared to wild-type mice. This could be attributed to impaired NF-κB activation, as shown by the absence of nuclear translocation of RelA with a decreased expression of IL-6, IL-12p40, and IL-17A. Remarkably, P0 -immunized TLR2 mice exhibited a delayed recovery as compared to TLR4 mice, which was because of an impaired T helper cell 2 polarization. Immunized TLR2 mice were unable to induce OX40 and OX40L by matrix metalloproteinase-2 on splenic dendritic cells. Subsequently, M2 polarization was impaired and macrophages were unable to sufficiently induce T regulatory cells (T ). Thus, in the recovery phase, T were significantly increased in TLR4 mice as compared to wild-type mice, whereas T in immunized TLR2 mice were only slightly increased. Our data highlight the relevance of innate immunity and, especially, the tight interaction between the innate and the adaptive immune system, which should be considered for therapeutic approaches of autoimmune diseases.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Fator 88 de Diferenciação Mieloide/metabolismo
Neurite Autoimune Experimental/metabolismo
Neurite Autoimune Experimental/patologia
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios/patologia
Linfócitos T CD4-Positivos/imunologia
Complemento C1q/imunologia
Progressão da Doença
Suscetibilidade a Doenças
Imunoglobulina G/sangue
Imunoglobulina M/sangue
Interferon gama/genética
Interferon gama/metabolismo
Contagem de Linfócitos
Ativação de Macrófagos
Metaloproteinase 2 da Matriz/metabolismo
Camundongos Endogâmicos C57BL
Músculo Esquelético/inervação
Músculo Esquelético/patologia
Proteína P0 da Mielina
NF-kappa B/metabolismo
Neurite Autoimune Experimental/sangue
Neurite Autoimune Experimental/imunologia
Ligante OX40/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores OX40/metabolismo
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Transdução de Sinais
Baço/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Immunoglobulin G); 0 (Immunoglobulin M); 0 (Myelin P0 Protein); 0 (Myeloid Differentiation Factor 88); 0 (NF-kappa B); 0 (OX40 Ligand); 0 (RNA, Messenger); 0 (Receptors, OX40); 0 (TICAM-1 protein, mouse); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 80295-33-6 (Complement C1q); 82115-62-6 (Interferon-gamma); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE


  10 / 553 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:27817222
[Au] Autor:Wang Y; Zhang J; Luo P; Zhu J; Feng J; Zhang HL
[Ad] Endereço:a Neuroscience Center, Department of Neurology , the First Hospital of Jilin University , Changchun , China.
[Ti] Título:Tumor necrosis factor-α in Guillain-Barré syndrome, friend or foe?
[So] Source:Expert Opin Ther Targets;21(1):103-112, 2017 Jan.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Guillain-Barré syndrome (GBS) is an immune-mediated disorder in the peripheral nervous system (PNS), and experimental autoimmune neuritis (EAN) serves as an animal model of GBS. TNF-α plays an important role in the pathogenesis of GBS and is a potential therapeutic target of GBS. Areas covered: 'TNF-α' and 'Guillain-Barré syndrome' were the keywords used to search for related publications on Pubmed. By binding to different TNF receptors, TNF-α bears distinct immune properties. TNF-α gene polymorphisms are associated with the features of GBS. The major role of TNF-α in GBS/EAN is to aggravate inflammation; however, data from several studies indicated a protective role of TNF-α. Multiple lines of evidence point to TNF-α as a potential therapeutic target for GBS. However, such clinical trials are scarce in that GBS per se is a probable side effect of anti-TNF-α treatment. Expert opinion: TNF-α plays a dual role in GBS and EAN, and is a potential therapeutic target on GBS/EAN.
[Mh] Termos MeSH primário: Síndrome de Guillain-Barré/tratamento farmacológico
Terapia de Alvo Molecular
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Síndrome de Guillain-Barré/fisiopatologia
Seres Humanos
Inflamação/patologia
Neurite Autoimune Experimental/tratamento farmacológico
Neurite Autoimune Experimental/fisiopatologia
Polimorfismo Genético
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE



página 1 de 56 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde