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[PMID]: 28049030 [Au] Autor: Daneshdoust D; Khalili-Fomeshi M; Ghasemi-Kasman M; Ghorbanian D; Hashemian M; Gholami M; Moghadamnia A; Shojaei A [Ad] Endereço: Student Research Committee, Faculty of Medical Sciences, Babol University of Medical Sciences, Babol, Mazandaran, Iran. [Ti] Título: Pregabalin enhances myelin repair and attenuates glial activation in lysolecithin-induced demyelination model of rat optic chiasm. [So] Source: Neuroscience;344:148-156, 2017 Mar 06. [Is] ISSN: 1873-7544 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Multiple sclerosis (MS) is an autoimmune disease in which more than 70% of patients experience visual disturbance as the earliest symptoms. Lysolecithin (LPC)-induced focal demyelination model has been developed to evaluate the effects of different therapies on myelin repair improvement. In this study, the effects of pregabalin administration on myelin repair and glial activation were investigated. Local demyelination was induced by administration of LPC (1%, 2µL) into the rat optic chiasm. Rats underwent daily injection of pregabalin (30mg/kg, i.p) or vehicle. Visual-evoked potentials (VEPs) recordings were performed for evaluating the function of optic pathway on days 3, 7, 14 and 28 post lesions. Myelin specific staining and immunostaining against GFAP and Iba1 were also carried out for assessment of myelination and glial activation respectively. Electrophysiological data indicated that pregabalin administration could significantly reduce the P1-N1 latency and increase the amplitude of VEPs waves compared to saline group. Luxol fast blue staining and immunostaining against PLP, as mature myelin marker, showed that myelin repair was improved in animals received pregabalin treatment. In addition, pregabalin effectively reduced the expression of GFAP and Iba1 as activated glial markers in optic chiasm. The present study indicates that pregabalin administration enhances myelin repair and ameliorates glial activation of optic chiasm following local injection of LPC. [Mh] Termos MeSH primário: Bainha de Mielina/efeitos dos fármacos Doença Autoimune do Sistema Nervoso Experimental/tratamento farmacológico Neuroglia/efeitos dos fármacos Fármacos Neuroprotetores/farmacologia Quiasma Óptico/efeitos dos fármacos Pregabalina/farmacologia [Mh] Termos MeSH secundário: Animais Proteínas de Ligação ao Cálcio/metabolismo Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/tratamento farmacológico Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/patologia Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/fisiopatologia Potenciais Evocados Visuais/efeitos dos fármacos Proteína Glial Fibrilar Ácida/metabolismo Lisofosfatidilcolinas Masculino Proteínas dos Microfilamentos/metabolismo Bainha de Mielina/patologia Bainha de Mielina/fisiologia Doença Autoimune do Sistema Nervoso Experimental/patologia Doença Autoimune do Sistema Nervoso Experimental/fisiopatologia Neuroglia/patologia Neuroglia/fisiologia Quiasma Óptico/patologia Quiasma Óptico/fisiopatologia Distribuição Aleatória Ratos Wistar [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Glial Fibrillary Acidic Protein); 0 (Lysophosphatidylcholines); 0 (Microfilament Proteins); 0 (Neuroprotective Agents); 0 (glial fibrillary acid protein, rat); 55JG375S6M (Pregabalin) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171109 [Lr] Data última revisão: 171109 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170104 [St] Status: MEDLINE

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[PMID]: 27621211 [Au] Autor: Diny NL; Hou X; Barin JG; Chen G; Talor MV; Schaub J; Russell SD; Klingel K; Rose NR; Ciháková D [Ad] Endereço: W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA. [Ti] Título: Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart. [So] Source: Eur J Immunol;46(12):2749-2760, 2016 Dec. [Is] ISSN: 1521-4141 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil-associated diseases. Eosinophils are thought to play a pathogenic role in myocarditis. We investigated the pathways that recruit eosinophils to the heart using a model of eosinophilic myocarditis, in which experimental autoimmune myocarditis (EAM) is induced in IFNγ IL-17A mice. Two conditions are necessary for efficient eosinophil trafficking to the heart: high eotaxin (CCL11, CCL24) expression in the heart and expression of the eotaxin receptor CCR3 by eosinophils. We identified cardiac fibroblasts as the source of CCL11 in the heart interstitium. CCL24 is produced by F4/80 macrophages localized at inflammatory foci in the heart. Expression of CCL11 and CCL24 is controlled by Th2 cytokines, IL-4 and IL-13. To determine the relevance of this pathway in humans, we analyzed endomyocardial biopsy samples from myocarditis patients. Expression of CCL11 and CCL26 was significantly increased in eosinophilic myocarditis compared to chronic lymphocytic myocarditis and positively correlated with the number of eosinophils. Thus, eosinophil trafficking to the heart is dependent on the eotaxin-CCR3 pathway in a mouse model of EAM and associated with cardiac eotaxin expression in patients with eosinophilic myocarditis. Blocking this pathway may prevent eosinophil-mediated cardiac damage. [Mh] Termos MeSH primário: Quimiocina CCL11/metabolismo Quimiocina CCL24/metabolismo Eosinófilos/imunologia Fibroblastos/imunologia Macrófagos/imunologia Miocardite/imunologia Miocárdio/imunologia Doença Autoimune do Sistema Nervoso Experimental/imunologia [Mh] Termos MeSH secundário: Adulto Idoso Animais Miosinas Cardíacas/imunologia Movimento Celular Células Cultivadas Feminino Seres Humanos Interferon gama/genética Masculino Camundongos Camundongos Endogâmicos BALB C Camundongos Knockout Camundongos Transgênicos Miocárdio/patologia Receptores CCR3/genética Equilíbrio Th1-Th2 [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Ccl11 protein, mouse); 0 (Ccl24 protein, mouse); 0 (Ccr3 protein, mouse); 0 (Chemokine CCL11); 0 (Chemokine CCL24); 0 (Receptors, CCR3); 82115-62-6 (Interferon-gamma); EC 3.6.1.- (Cardiac Myosins) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 170705 [Lr] Data última revisão: 170705 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160914 [St] Status: MEDLINE [do] DOI: 10.1002/eji.201646557

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[PMID]: 27577085 [Au] Autor: Sinmaz N; Nguyen T; Tea F; Dale RC; Brilot F [Ad] Endereço: Brain Autoimmunity Group, Institute for Neuroscience and Muscle Research, The Kids Research Institute at the Children's Hospital at Westmead, University of Sydney, Locked Bag 4001, Westmead, NSW, 2145, Australia. [Ti] Título: Mapping autoantigen epitopes: molecular insights into autoantibody-associated disorders of the nervous system. [So] Source: J Neuroinflammation;13(1):219, 2016 Aug 30. [Is] ISSN: 1742-2094 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: BACKGROUND: Our knowledge of autoantibody-associated diseases of the central (CNS) and peripheral (PNS) nervous systems has expanded greatly over the recent years. A number of extracellular and intracellular autoantigens have been identified, and there is no doubt that this field will continue to expand as more autoantigens are discovered as a result of improved clinical awareness and methodological practice. In recent years, interest has shifted to uncover the target epitopes of these autoantibodies. MAIN BODY: The purpose of this review is to discuss the mapping of the epitope targets of autoantibodies in CNS and PNS antibody-mediated disorders, such as N-methyl-D-aspartate receptor (NMDAR), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), leucine-rich glioma-inactivated protein 1 (Lgi1), contactin-associated protein-like 2 (Caspr2), myelin oligodendrocyte glycoprotein (MOG), aquaporin-4 (AQP4), 65 kDa glutamic acid decarboxylase (GAD65), acetylcholine receptor (AChR), muscle-specific kinase (MuSK), voltage-gated calcium channel (VGCC), neurofascin (NF), and contactin. We also address the methods used to analyze these epitopes, the relevance of their determination, and how this knowledge can inform studies on autoantibody pathogenicity. Furthermore, we discuss triggers of autoimmunity, such as molecular mimicry, ectopic antigen expression, epitope spreading, and potential mechanisms for the rising number of double autoantibody-positive patients. CONCLUSIONS: Molecular insights into specificity and role of autoantibodies will likely improve diagnosis and treatment of CNS and PNS neuroimmune diseases. [Mh] Termos MeSH primário: Autoanticorpos/imunologia Autoantígenos/imunologia Doenças Autoimunes do Sistema Nervoso/imunologia Mapeamento de Epitopos/métodos Epitopos/imunologia [Mh] Termos MeSH secundário: Animais Autoanticorpos/metabolismo Autoantígenos/metabolismo Doenças Autoimunes do Sistema Nervoso/metabolismo Epitopos/metabolismo Seres Humanos Doença Autoimune do Sistema Nervoso Experimental/imunologia Doença Autoimune do Sistema Nervoso Experimental/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Autoantibodies); 0 (Autoantigens); 0 (Epitopes) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171009 [Lr] Data última revisão: 171009 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160901 [St] Status: MEDLINE [do] DOI: 10.1186/s12974-016-0678-4

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[PMID]: 26919582 [Au] Autor: Liang D; Zuo A; Zhao R; Shao H; Born WK; O'Brien RL; Kaplan HJ; Sun D [Ad] Endereço: Doheny Eye Institute and Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, California 90033, United States of America. [Ti] Título: CD73 Expressed on γδ T Cells Shapes Their Regulatory Effect in Experimental Autoimmune Uveitis. [So] Source: PLoS One;11(2):e0150078, 2016. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: γδ T cells can either enhance or inhibit an adaptive immune response, but the mechanisms involved are not fully understood. Given that CD73 is the main enzyme responsible for conversion of AMP into the immunosuppressive molecule adenosine, we investigated its role in the regulatory function of γδ T cells in experimental autoimmune uveitis (EAU). We found that γδ T cells expressed different amounts of CD73 during the different stages of EAU and that low CD73 expression on γδ T cells correlated with enhanced Th17 response-promoting activity. Functional comparison of CD73-deficient and wild-type B6 (CD73+/+) mice showed that failure to express CD73 decreased both the enhancing and suppressive effects of γδ T cells on EAU. We also demonstrated that γδ T cells expressed different amounts of CD73 when activated by different pathways, which enabled them to either enhance or inhibit an adaptive immune response. Our results demonstrate that targeting CD73 expression on γδ T cells may allow us to manipulate their pro- or anti-inflammatory effect on Th17 responses. [Mh] Termos MeSH primário: 5´-Nucleotidase/fisiologia Doença Autoimune do Sistema Nervoso Experimental/imunologia Subpopulações de Linfócitos T/imunologia Linfócitos T Reguladores/imunologia Uveíte/imunologia [Mh] Termos MeSH secundário: 5'-Nucleotidase/biossíntese 5'-Nucleotidase/deficiência 5'-Nucleotidase/genética Adenosina/metabolismo Monofosfato de Adenosina/metabolismo Animais Células Cultivadas Células Dendríticas/imunologia Proteínas do Olho/imunologia Proteínas do Olho/toxicidade Feminino Regulação da Expressão Gênica/imunologia Interferon gama/sangue Interferon gama/deficiência Interleucina-17/sangue Ativação Linfocitária Camundongos Camundongos Endogâmicos C57BL Camundongos Knockout Doença Autoimune do Sistema Nervoso Experimental/enzimologia Fragmentos de Peptídeos/imunologia Fragmentos de Peptídeos/toxicidade Receptores de Antígenos de Linfócitos T gama-delta/análise Receptores de Antígenos de Linfócitos T gama-delta/deficiência Proteínas de Ligação ao Retinol/imunologia Proteínas de Ligação ao Retinol/toxicidade Subpopulações de Linfócitos T/enzimologia Linfócitos T Reguladores/enzimologia Células Th1/imunologia Células Th17/imunologia Uveíte/enzimologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Eye Proteins); 0 (Interleukin-17); 0 (Peptide Fragments); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Retinol-Binding Proteins); 0 (interstitial retinol-binding protein); 415SHH325A (Adenosine Monophosphate); 82115-62-6 (Interferon-gamma); EC 3.1.3.5 (5'-Nucleotidase); K72T3FS567 (Adenosine) [Em] Mês de entrada: 1607 [Cu] Atualização por classe: 170719 [Lr] Data última revisão: 170719 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160227 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0150078

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[PMID]: 26475067 [Au] Autor: Takamura C; Suzuki J; Ogawa M; Watanabe R; Tada Y; Maejima Y; Akazawa H; Komuro I; Isobe M [Ad] Endereço: Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan. [Ti] Título: Suppression of murine autoimmune myocarditis achieved with direct renin inhibition. [So] Source: J Cardiol;68(3):253-60, 2016 09. [Is] ISSN: 1876-4738 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: BACKGROUND: The renin angiotensin system (RAS) plays an important role in the pathogenesis of cardiovascular diseases and inflammation. Myocarditis is an inflammatory disease of the heart, and the role of the RAS in its pathophysiology is unknown. Because the direct renin inhibitor, aliskiren, is thought to block RAS completely, we investigated the cardioprotective effect of aliskiren in mice with experimental autoimmune myocarditis (EAM). METHODS: A cardiac α-myosin heavy chain peptide was injected in mice on days 0 and 7. Aliskiren 25mg/kg per day (n=10) or vehicle (n=10) was administered to EAM mice starting on day 0 and the animals were killed on day 21. RESULTS: Aliskiren significantly prevented the progression of left ventricular wall thickening in EAM hearts compared to the vehicle-treated group. Histologically, the inflammatory cell infiltration and fibrosis area ratios in the aliskiren-treated group were lower than that in the vehicle-treated group. Immunohistochemistry revealed that aliskiren suppressed CD4 positive cell infiltration in EAM hearts compared to vehicle. Moreover, aliskiren decreased mRNA levels of interleukin (IL)-2, interferon-γ, tumor necrosis factor-α, and collagen 1. In vitro study showed that aliskiren inhibited T cell proliferation and IL-2 production induced by myosin stimulation. CONCLUSION: Our results suggest that aliskiren ameliorates EAM by suppressing T-cell activation and inflammatory cytokines, and has potential as a treatment for myocarditis. [Mh] Termos MeSH primário: Amidas/farmacologia Anti-Hipertensivos/farmacologia Fumaratos/farmacologia Doença Autoimune do Sistema Nervoso Experimental/tratamento farmacológico Renina/antagonistas & inibidores [Mh] Termos MeSH secundário: Animais Citocinas/genética Citocinas/metabolismo Ativação Linfocitária/efeitos dos fármacos Camundongos Camundongos Endogâmicos BALB C RNA Mensageiro/efeitos dos fármacos RNA Mensageiro/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Amides); 0 (Antihypertensive Agents); 0 (Cytokines); 0 (Fumarates); 0 (RNA, Messenger); 502FWN4Q32 (aliskiren); EC 3.4.23.15 (Renin) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 171103 [Lr] Data última revisão: 171103 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 151018 [St] Status: MEDLINE

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[PMID]: 26337870 [Au] Autor: James RE; Hillis J; Adorján I; Gration B; Mundim MV; Iqbal AJ; Majumdar MM; Yates RL; Richards MM; Goings GE; DeLuca GC; Greaves DR; Miller SD; Szele FG [Ad] Endereço: Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, OX1 3HS, United Kingdom. [Ti] Título: Loss of galectin-3 decreases the number of immune cells in the subventricular zone and restores proliferation in a viral model of multiple sclerosis. [So] Source: Glia;64(1):105-21, 2016 Jan. [Is] ISSN: 1098-1136 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Multiple sclerosis (MS) frequently starts near the lateral ventricles, which are lined by subventricular zone (SVZ) progenitor cells that can migrate to lesions and contribute to repair. Because MS-induced inflammation may decrease SVZ proliferation and thus limit repair, we studied the role of galectin-3 (Gal-3), a proinflammatory protein. Gal-3 expression was increased in periventricular regions of human MS in post-mortem brain samples and was also upregulated in periventricular regions in a murine MS model, Theiler's murine encephalomyelitis virus (TMEV) infection. Whereas TMEV increased SVZ chemokine (CCL2, CCL5, CCL, and CXCL10) expression in wild type (WT) mice, this was inhibited in Gal-3(-/-) mice. Though numerous CD45+ immune cells entered the SVZ of WT mice after TMEV infection, their numbers were significantly diminished in Gal-3(-/-) mice. TMEV also reduced neuroblast and proliferative SVZ cell numbers in WT mice but this was restored in Gal-3(-/-) mice and was correlated with increased numbers of doublecortin+ neuroblasts in the corpus callosum. In summary, our data showed that loss of Gal-3 blocked chemokine increases after TMEV, reduced immune cell migration into the SVZ, reestablished SVZ proliferation and increased the number of progenitors in the corpus callosum. These results suggest Gal-3 plays a central role in modulating the SVZ neurogenic niche's response to this model of MS. [Mh] Termos MeSH primário: Encéfalo/metabolismo Galectina 3/metabolismo Esclerose Múltipla/metabolismo Doença Autoimune do Sistema Nervoso Experimental/metabolismo Neurogênese Nicho de Células-Tronco/fisiologia [Mh] Termos MeSH secundário: Adolescente Adulto Idoso Animais Encéfalo/imunologia Encéfalo/patologia Movimento Celular Criança Feminino Galectina 3/genética Seres Humanos Masculino Camundongos Endogâmicos C57BL Camundongos Knockout Meia-Idade Esclerose Múltipla/imunologia Esclerose Múltipla/patologia Doença Autoimune do Sistema Nervoso Experimental/imunologia Doença Autoimune do Sistema Nervoso Experimental/patologia Células-Tronco Neurais/metabolismo Células-Tronco Neurais/patologia Poliomielite/metabolismo Poliomielite/patologia Theilovirus Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Galectin 3) [Em] Mês de entrada: 1610 [Cu] Atualização por classe: 171110 [Lr] Data última revisão: 171110 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150905 [St] Status: MEDLINE [do] DOI: 10.1002/glia.22906

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[PMID]: 26823763 [Au] Autor: Kang J; Zhang HY; Feng GD; Feng DY; Jia HG [Ad] Endereço: Department of Neurology, Xijing Hospital, The Fourth Military Medical University Xi'an, Shaanxi, China. [Ti] Título: Development of an improved animal model of experimental autoimmune myositis. [So] Source: Int J Clin Exp Pathol;8(11):14457-64, 2015. [Is] ISSN: 1936-2625 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Multiple animal models of experimental autoimmune myositis (EAM) have been developed. However, these models vary greatly in the severity of disease and reproducibility. The goal of this study was to test whether vaccination twice with increased dose of rat myosin and pertussis toxin (PT) could induce EAM with severer disease in mice. BALB/c mice were injected with 1 mg rat myosin in 50% complete Freund's adjuvant (CFA) weekly for four times and one time of PT (EAM) or twice with 1.5 mg myosin in CFA and PT (M-EAM). In comparison with that in the CFA and PT injected controls, vaccination with rat myosin and injection PT significantly reduced the muscle strength and EMG duration, elevated serum creatine kinase levels, promoted inflammatory infiltration in the muscle tissues, leading to pathological changes in the muscle tissues, demonstrating to induce EAM. Interestingly, we found that vaccination twice with the high dose of myosin and PT prevented EAM-related gain in body weights and caused significantly less muscle strength in mice. More importantly, all of the mice receiving high dose of myosin and PT survived while 3 out of 16 mice with four times of low dose of myosin died. Finally, vaccination with high dose of myosin promoted CD4(+) and CD8(+) T cell infiltration in the muscle tissues and up-regulated MHC-I expression in the muscle tissues of mice. Hence, the new model of EAM is a time-saving, efficient and easily replicable tool for studying autoimmune myositis. [Mh] Termos MeSH primário: Miosinas Doença Autoimune do Sistema Nervoso Experimental/induzido quimicamente Toxina Pertussis [Mh] Termos MeSH secundário: Animais Biomarcadores/sangue Linfócitos T CD4-Positivos/imunologia Linfócitos T CD8-Positivos/imunologia Quimiotaxia de Leucócito Creatina Quinase Forma MM/sangue Progressão da Doença Feminino Cobaias Camundongos Endogâmicos BALB C Força Muscular Músculo Esquelético/imunologia Músculo Esquelético/metabolismo Músculo Esquelético/patologia Músculo Esquelético/fisiopatologia Doença Autoimune do Sistema Nervoso Experimental/sangue Doença Autoimune do Sistema Nervoso Experimental/imunologia Doença Autoimune do Sistema Nervoso Experimental/patologia Doença Autoimune do Sistema Nervoso Experimental/fisiopatologia Fenótipo Índice de Gravidade de Doença Fatores de Tempo Ganho de Peso [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Biomarkers); EC 2.4.2.31 (Pertussis Toxin); EC 2.7.3.2 (Creatine Kinase, MM Form); EC 3.6.4.1 (Myosins) [Em] Mês de entrada: 1610 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160130 [St] Status: MEDLINE

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[PMID]: 26318182 [Au] Autor: Liu Y; You C; Zhang Z; Zhang J; Yan H [Ad] Endereço: Department of Ophthalmology, Tianjin Medical University General Hospital, No. 154, Anshan Road, Tianjin, 300052, China. [Ti] Título: Roles of Treg/Th17 Cell Imbalance and Neuronal Damage in the Visual Dysfunction Observed in Experimental Autoimmune Optic Neuritis Chronologically. [So] Source: Neuromolecular Med;17(4):391-403, 2015 Dec. [Is] ISSN: 1559-1174 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Optic neuritis associated with multiple sclerosis and its animal model, experimental autoimmune optic neuritis (EAON), is characterized by inflammation, T cell activation, demyelination, and neuronal damage, which might induce permanent vision loss. Elucidating the chronological relationship among the features is critical for treatment of demyelinating optic neuritis. EAON was induced in C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein subcutaneously, and visual function was assessed by flash-visual evoked potential (F-VEP) at days 7, 11, 14, 19, 23, 28 post-immunization. Retinal ganglion cell (RGC) apoptosis was measured by terminal-deoxynucleotidyl transferase-mediated nick-end labeling. Demyelination and axonal damage were verified with myelin basic protein (MBP) and ß-amyloid precursor protein staining, respectively. Real-time polymerase chain reaction quantified IL-17, IL-1ß, TGF-ß, FoxP3, IL-6, and IL-10 mRNA expression in the optic nerve, as well as FoxP3 and IL-17 staining. Systemic changes of Th17 and Treg cells were tested by flow cytometry in spleen. F-VEP latency was prolonged at 11 days and peaked at 23 days commensurate with demyelination. However, F-VEP amplitude was reduced at 11 days, preceding axon damage, and was exacerbated at 23 days when a peak in RGC apoptosis was detected. Th17 cells up-regulated as early as 7 days and peaked at 11 days, while Treg cells down-regulated inversely compared to Th17 cells change as verified by IL-17 and FoxP3 expression; spleen cell samples were slightly different, demonstrating marked changed at 14 days. Treg/Th17 cell imbalance in the optic nerve precedes and may initiate neuronal damage of axons and RGCs. These changes are commensurate with the appearances of visual dysfunction reflected in F-VEP and hence may offer a novel therapeutic avenue for vision preservation. [Mh] Termos MeSH primário: Doença Autoimune do Sistema Nervoso Experimental/imunologia Neurite Óptica/imunologia Células Ganglionares da Retina/patologia Linfócitos T Reguladores/imunologia Células Th17/imunologia [Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/análise Animais Apoptose Axônios/patologia Doenças Desmielinizantes Potenciais Evocados Visuais Feminino Fatores de Transcrição Forkhead/biossíntese Fatores de Transcrição Forkhead/genética Interleucinas/biossíntese Interleucinas/genética Contagem de Linfócitos Linfotoxina-alfa/biossíntese Linfotoxina-alfa/genética Camundongos Camundongos Endogâmicos C57BL Proteína Básica da Mielina/análise Proteínas do Tecido Nervoso/biossíntese Proteínas do Tecido Nervoso/genética Doença Autoimune do Sistema Nervoso Experimental/sangue Doença Autoimune do Sistema Nervoso Experimental/patologia Nervo Óptico/metabolismo Nervo Óptico/patologia Neurite Óptica/sangue Neurite Óptica/patologia Células Ganglionares da Retina/química Linfócitos T Reguladores/patologia Células Th17/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Amyloid beta-Protein Precursor); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Interleukins); 0 (Lymphotoxin-alpha); 0 (Myelin Basic Protein); 0 (Nerve Tissue Proteins) [Em] Mês de entrada: 1609 [Cu] Atualização por classe: 171107 [Lr] Data última revisão: 171107 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150831 [St] Status: MEDLINE [do] DOI: 10.1007/s12017-015-8368-4

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[PMID]: 26016323 [Au] Autor: Morozova MP; Lukoshkova EV; Gavrilova SA [Ti] Título: [Some aspects of heart rate variability estimation in rats]. [So] Source: Ross Fiziol Zh Im I M Sechenova;101(3):291-307, 2015 Mar. [Is] ISSN: 0869-8139 [Cp] País de publicação: Russia (Federation) [La] Idioma: rus [Ab] Resumo: This study focuses on researching of heart rate variability (HRV) in rats with autoimmune myocarditis. Intact rats were investigated additionally. It was registered 2-, 5- and 20-min duration ECG from awake animals at rest-conditions and after cooling probe (CP), and then time domain and spectral parameters of HRV were calculated. We shown that 1) after CP decreasing of parasympathetic influence and augmentation of sympathetic influence on heart rate regulation in rats with autoimmune myocarditis was more manifested than in intact rats, 2) in CP with the 5-min ECG interval's duration was more informative for HRV estimation, 3) intracardiac inflammation leads to modification of correlation interconnection between some HRV-parameters, and that may talk about features of heart's chronotropic regulation in rats with autoimmune myocarditis. [Mh] Termos MeSH primário: Frequência Cardíaca/fisiologia Doença Autoimune do Sistema Nervoso Experimental/fisiopatologia Descanso/fisiologia [Mh] Termos MeSH secundário: Animais Masculino Ratos Análise de Regressão [Pt] Tipo de publicação: ENGLISH ABSTRACT; JOURNAL ARTICLE [Em] Mês de entrada: 1506 [Cu] Atualização por classe: 161020 [Lr] Data última revisão: 161020 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150529 [St] Status: MEDLINE

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[PMID]: 25580817 [Au] Autor: Kimura N; Hirata S; Miyasaka N; Kawahata K; Kohsaka H [Ad] Endereço: Tokyo Medical and Dental University, Tokyo, Japan. [Ti] Título: Injury and subsequent regeneration of muscles for activation of local innate immunity to facilitate the development and relapse of autoimmune myositis in C57BL/6 mice. [So] Source: Arthritis Rheumatol;67(4):1107-16, 2015 Apr. [Is] ISSN: 2326-5205 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: OBJECTIVE: To determine whether injury and regeneration of the skeletal muscles induce an inflammatory milieu that facilitates the development and relapse of autoimmune myositis. METHODS: The quadriceps of C57BL/6 mice were injured with bupivacaine hydrochloride (BPVC) and evaluated histologically. Macrophages and regenerating myofibers in the treated muscles and differentiating C2C12 myotubes were examined for cytokine expression. Mice were immunized with C protein fragments at the base of the tail and in the right hind footpads (day 0) to evoke systemic anti-C protein immunity and to induce local myositis in the right hind limbs. The contralateral quadriceps muscles were injured with BPVC or phosphate buffered saline (PBS) on day 7 or after spontaneous regression of myositis (day 42). The quadriceps muscle in nonimmunized mice was injured with BPVC on day 7. The muscles were examined histologically 14 days after treatment. RESULTS: The BPVC-injured muscles had macrophage infiltration most abundantly at 3 days after the injection, with emergence of regenerating fibers from day 5. The macrophages expressed inflammatory cytokines, including tumor necrosis factor α, interleukin-1ß, and CCL2. Regenerating myofibers and C2C12 myotubes also expressed the cytokines. The BPVC-injected muscles from nonimmunized mice had regenerating myofibers with resolved cell infiltration 14 days after treatment. In mice preimmunized with C protein fragments, the muscles injected with BPVC on day 7 as well as on day 42, but not those injected with PBS, had myositis accompanied by CD8+ T cell infiltration. CONCLUSION: Injury and regeneration could set up an inflammatory milieu in the muscles and facilitate the development and relapse of autoimmune myositis. [Mh] Termos MeSH primário: Imunidade Inata Músculo Esquelético/imunologia Miosite/imunologia Doença Autoimune do Sistema Nervoso Experimental/imunologia Regeneração/imunologia [Mh] Termos MeSH secundário: Animais Citocinas/metabolismo Camundongos Camundongos Endogâmicos C57BL Músculo Esquelético/metabolismo Miosite/metabolismo Doença Autoimune do Sistema Nervoso Experimental/metabolismo Recidiva [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Cytokines) [Em] Mês de entrada: 1505 [Cu] Atualização por classe: 160511 [Lr] Data última revisão: 160511 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 150113 [St] Status: MEDLINE [do] DOI: 10.1002/art.39017

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