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1.
Neurosci Lett ; 736: 135295, 2020 09 25.
Artigo em Inglês | MEDLINE | ID: mdl-32800922

RESUMO

Herpes simplex virus type 1 (HSV-1) is the main etiological agent of acute and sporadic encephalitis. Proteins of the suppressor of cytokine signaling (SOCS) family have shown to regulate the inflammation during HSV-1 infection in the brain. However, the effects of SOCS2 and SOCS3 in viral encephalitis remain unclear. The aim of the current study is to investigate the potential association between SOCS2, SOCS3, cytokines, and hippocampal damage, especially neuronal apoptosis, during acute intracranial HSV-1 infection in mice. Male C57BL/6 mice were infected by intracranial route with 102 plaque-forming units (PFU) inoculum of purified HSV-1. At three days post-infection (3 d.p.i.), mice were euthanized and their hippocampi were collected for histopathological analysis, immunohistochemical reaction against active caspase-3 and quantification of SOCS2, SOCS3 and cytokines (tumoral necrosis factor (TNF), interleukin (IL) 1ß, IL-6, IL-10; interferon (IFN) -α, IFN-ß, IFN-γ) mRNA expression. Infected mice exhibited neuronal loss and hemorrhagic focus in Cornu Ammonis (CA) region. The apoptotic index was higher in infected mice compared to controls. HSV-1 infection was associated with increased hippocampal expression of TNF, IL1-ß, IL-6 and IFNα/IFNß and decreased expression of IL-10, IFN-γ, SOCS2 and SOCS3. Our results suggest that down regulation of SOCS2 and SOCS3 contributes to a pro-inflammatory environment associated with hippocampal damage and neuronal apoptosis during acute HSV-1 infection in mice.


Assuntos
Encefalite por Herpes Simples/metabolismo , Hipocampo/virologia , Inflamação/metabolismo , Proteína 3 Supressora da Sinalização de Citocinas/metabolismo , Proteínas Supressoras da Sinalização de Citocina/metabolismo , Animais , Apoptose/fisiologia , Chlorocebus aethiops , Citocinas/metabolismo , Hipocampo/metabolismo , Masculino , Camundongos , Neurônios/metabolismo , Neurônios/virologia , Células Vero
2.
J Neuroimmunol ; 278: 69-72, 2015 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-25595254

RESUMO

The pathogenesis of autism spectrum disorder (ASD) is unknown, and the immune system has been appointed to play an important role. The interleukin 33 (IL-33), a member of the IL-1, may act as an alarmin. This study aimed to evaluate plasma levels of IL-33, sST2, and IL-1ß in 30 patients with ASD in comparison with 18 controls matched by gender, age and maternal age at childbirth. Patients did not differ from controls in IL-33, sST2, and IL-1ß plasma levels. Alarmin levels were not correlated with age, and neither was influenced by clinical parameters. Our results undermine the role of IL-33/ST2 in ASD.


Assuntos
Transtornos Globais do Desenvolvimento Infantil/sangue , Interleucinas/sangue , Adolescente , Estudos de Casos e Controles , Criança , Transtornos Globais do Desenvolvimento Infantil/complicações , Feminino , Humanos , Proteína 1 Semelhante a Receptor de Interleucina-1 , Interleucina-1beta/sangue , Interleucina-33 , Masculino , Escalas de Graduação Psiquiátrica , Receptores de Superfície Celular/sangue , Estatísticas não Paramétricas
3.
Neuro Endocrinol Lett ; 35(5): 380-4, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25275256

RESUMO

OBJECTIVES: Evaluate the levels of a neurotrophic factor and some neurotrophins in the plasma of patients with Autism Spectrum Disorders (ASD). DESIGN: This study enrolled 30 children with ASD and 19 healthy children. Plasma levels of the neurotrophins BDNF, NGF, NT3, NT4 and of the neurotrophic factor GDNF were measured by Enzyme-Linked Immunosorbent Assay. SETTING: The etiopathogenesis of ASD is largely unknown, but it seems to involve dysfunction in several biological systems. One of these systems comprises the neurotrophic factors, which are molecules involved in many processes in the central nervous system, including neuronal survival, synaptogenesis and synaptic plasticity. Recent studies have shown association between neurotrophic factors and ASD. RESULTS: No differences in plasma BDNF, NGF, NT3, NT4 and GDNF were found between ASD and control. Neurotrophic factors are not altered in ASD. CONCLUSIONS: These molecules may play a minor role in ASD.


Assuntos
Transtornos Globais do Desenvolvimento Infantil/sangue , Transtornos Globais do Desenvolvimento Infantil/epidemiologia , Fatores de Crescimento Neural/sangue , Adolescente , Adulto , Fator Neurotrófico Derivado do Encéfalo/sangue , Criança , Pré-Escolar , Feminino , Fator Neurotrófico Derivado de Linhagem de Célula Glial/sangue , Humanos , Masculino , Idade Materna , Pessoa de Meia-Idade , Fator de Crescimento Neural/sangue , Plasticidade Neuronal/fisiologia , Neurotrofina 3/sangue , Fatores de Risco , Adulto Jovem
4.
Neuropsychobiology ; 69(1): 6-10, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24401207

RESUMO

BACKGROUND AND OBJECTIVE: The etiopathogenesis of autism spectrum disorders (ASD) is largely unknown, but it seems to involve dysfunction in several biological systems. Among many possible biological pathways, the immune system has emerged as potentially involved. Recent studies have shown association between cytokines (molecules that mediate immune cell interaction) and ASD. Adipokines are cytokines secreted mainly by adipose tissue and may have systemic effects. The main objective of this study was to compare the plasma levels of three adipokines between patients with ASD and healthy controls. Another aim was to correlate the levels of these adipokines and the severity of autistic symptoms as measured by the Social Responsiveness Scale (SRS). METHODS: We collected plasma from 30 patients and 19 controls and measured the levels of adiponectin, leptin and resistin using a commercially available kit. We also used the SRS as a tool to assess the severity of autistic symptoms. RESULTS: We found decreased levels of resistin, increased levels of leptin and unaltered levels of adiponectin in plasma from ASD subjects in comparison with controls. There was also a negative correlation between the levels of adiponectin and the severity of symptoms as assessed by the SRS. CONCLUSION: There are significant changes in the plasma levels of adipokines from patients with ASDs. They suggest the occurrence of systemic changes in ASD and may be hallmarks of the disease.


Assuntos
Adiponectina/sangue , Transtornos Globais do Desenvolvimento Infantil/sangue , Leptina/sangue , Resistina/sangue , Estudos de Casos e Controles , Criança , Humanos , Índice de Gravidade de Doença
5.
Clinics (Sao Paulo) ; 68(3): 391-4, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23644861

RESUMO

OBJECTIVE: Ischemic stroke may result from transient or permanent reductions of regional cerebral blood flow. Polymorphonuclear neutrophils have been described as the earliest inflammatory cells to arrive in ischemic tissue. CXCR1/2 receptors are involved in the recruitment of these cells. However, the contribution of these chemokine receptors during transient brain ischemia in mice remains poorly understood. In this work, we investigated the effects of reparixin, an allosteric antagonist of CXCR1/2 receptors, in a model of middle cerebral artery occlusion and reperfusion in mice. METHODS: C57BL/6J male mice treated with reparixin or vehicle were subjected to a middle cerebral artery occlusion procedure 1 h after the treatment. Ninety minutes after ischemia induction, the monofilament that prevented blood flow was removed. Twenty-four hours after the reperfusion procedure, behavioral changes, including motor signs, were analyzed with the SmithKline/Harwell/lmperial College/Royal Hospital/Phenotype Assessment (SHIRPA) battery. The animals were sacrificed, and brain tissue was removed for histological and biochemical analyses. Histological sections were stained with hematoxylin and eosin, neutrophil infiltration was estimated by myeloperoxidase activity and the inflammatory cytokine IL-iß was measured by ELISA. RESULTS: Pre-treatment with reparixin reduced the motor deficits observed in this model of ischemia and reperfusion. Myeloperoxidase activity and IL-iß were reduced in the reparixin-treated group. Histological analysis revealed that ischemic injury was also attenuated by reparixin pre-treatment. CONCLUSIONS: Our results suggest that the blockade of the CXCR1/2 receptors by reparixin promotes neuroprotective effects by reducing the levels of polymorphonuclear infiltration in the brain and the tissue damage associated with middle cerebral artery occlusion and reperfusion.


Assuntos
Lesões Encefálicas/prevenção & controle , Isquemia Encefálica/tratamento farmacológico , Fármacos Neuroprotetores/uso terapêutico , Receptores de Interleucina-8A/antagonistas & inibidores , Receptores de Interleucina-8B/antagonistas & inibidores , Acidente Vascular Cerebral/tratamento farmacológico , Sulfonamidas/uso terapêutico , Animais , Lesões Encefálicas/tratamento farmacológico , Ensaio de Imunoadsorção Enzimática , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fármacos Neuroprotetores/farmacologia , Peroxidase/metabolismo , Reprodutibilidade dos Testes , Sulfonamidas/farmacologia , Fatores de Tempo , Resultado do Tratamento
6.
Clinics ; 68(3): 391-394, 2013. ilus, graf
Artigo em Inglês | LILACS | ID: lil-671432

RESUMO

OBJECTIVE: Ischemic stroke may result from transient or permanent reductions of regional cerebral blood flow. Polymorphonuclear neutrophils have been described as the earliest inflammatory cells to arrive in ischemic tissue. CXCR1/2 receptors are involved in the recruitment of these cells. However, the contribution of these chemokine receptors during transient brain ischemia in mice remains poorly understood. In this work, we investigated the effects of reparixin, an allosteric antagonist of CXCR1/2 receptors, in a model of middle cerebral artery occlusion and reperfusion in mice. METHODS: C57BL/6J male mice treated with reparixin or vehicle were subjected to a middle cerebral artery occlusion procedure 1 h after the treatment. Ninety minutes after ischemia induction, the monofilament that prevented blood flow was removed. Twenty-four hours after the reperfusion procedure, behavioral changes, including motor signs, were analyzed with the SmithKline/Harwell/lmperial College/Royal Hospital/Phenotype Assessment (SHIRPA) battery. The animals were sacrificed, and brain tissue was removed for histological and biochemical analyses. Histological sections were stained with hematoxylin and eosin, neutrophil infiltration was estimated by myeloperoxidase activity and the inflammatory cytokine IL-iβ was measured by ELISA. RESULTS: Pre-treatment with reparixin reduced the motor deficits observed in this model of ischemia and reperfusion. Myeloperoxidase activity and IL-iβ were reduced in the reparixin-treated group. Histological analysis revealed that ischemic injury was also attenuated by reparixin pre-treatment. CONCLUSIONS: Our results suggest that the blockade of the CXCR1/2 receptors by reparixin promotes neuroprotective effects by reducing the levels of polymorphonuclear infiltration in the brain and the tissue damage associated with middle cerebral artery occlusion and reperfusion.


Assuntos
Animais , Masculino , Camundongos , Lesões Encefálicas/prevenção & controle , Isquemia Encefálica/tratamento farmacológico , Fármacos Neuroprotetores/uso terapêutico , /antagonistas & inibidores , /antagonistas & inibidores , Acidente Vascular Cerebral/tratamento farmacológico , Sulfonamidas/uso terapêutico , Lesões Encefálicas/tratamento farmacológico , Ensaio de Imunoadsorção Enzimática , Fármacos Neuroprotetores/farmacologia , Peroxidase/metabolismo , Reprodutibilidade dos Testes , Sulfonamidas/farmacologia , Fatores de Tempo , Resultado do Tratamento
7.
Arq. neuropsiquiatr ; 69(6): 938-942, Dec. 2011. graf
Artigo em Inglês | LILACS | ID: lil-612637

RESUMO

Multiple sclerosis is a neuroinflammatory disease that results in serious neurological disability. Besides physical impairment, behavioral symptoms are also common in patients with multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is considered to be a model of multiple sclerosis and mimics the main features of the disease, such as demyelination and motor impairment. In this work, we aimed to study behavioral parameters in animals with EAE using the MOG35-55 model in C57BL/6 mice. We analyzed memory and anxiety in animals using the elevated plus maze, the step down inhibitory avoidance task and the memory recognition test. No differences in any tests were found when comparing controls and animals induced with EAE. Therefore, we conclude that behavioral changes in animals with EAE induced with MOG35-55 are probably subtle or absent.


Esclerose múltipla é uma doença neuroinflamatória que resulta em séria incapacidade neurológica. Além do comprometimento físico, sintomas comportamentais também são comuns em pacientes com esclerose múltipla. A encefalomielite autoimune experimental (EAE) é considerada um modelo de esclerose múltipla e mimetiza as principais caracte-rísticas da doença, como a desmielinização e a fraqueza motora. Neste trabalho, objetivamos estudar parâmetros comportamentais em animais com EAE usando o modelo de MOG35-55 em camundongos C57BL/6. Analisamos memória e ansiedade em animais utilizando o labirinto em cruz elevado, o teste da esquiva inibitória e o teste de memória de reconhecimento. Nenhuma diferença em quaisquer dos testes foi encontrada comparando animais controles e animais induzidos com EAE. Assim, concluímos que alterações comportamentais em animais com EAE induzidos com MOG35-55 são provavelmente sutis ou ausentes.


Assuntos
Animais , Feminino , Camundongos , Ansiedade/psicologia , Comportamento Animal/fisiologia , Modelos Animais de Doenças , Encefalomielite Autoimune Experimental/psicologia , Memória/fisiologia , Ansiedade/fisiopatologia , Aprendizagem da Esquiva/fisiologia , Encefalomielite Autoimune Experimental/fisiopatologia , Aprendizagem em Labirinto/fisiologia
8.
J Immunol ; 187(7): 3821-30, 2011 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-21890656

RESUMO

Rheumatoid arthritis (RA) and periodontal disease (PD) are prevalent chronic inflammatory disorders that affect bone structures. Individuals with RA are more likely to experience PD, but how disease in joints could induce PD remains unknown. This study aimed to experimentally mimic clinical parameters of RA-induced PD and to provide mechanistic findings to explain this association. Chronic Ag-induced arthritis (AIA) was triggered by injection of methylated BSA in the knee joint of immunized mice. Anti-TNF-α was used to assess the role of this cytokine. Intra-articular challenge induced infiltration of cells, synovial hyperplasia, bone resorption, proteoglycan loss, and increased expression of cytokines exclusively in challenged joints. Simultaneously, AIA resulted in severe alveolar bone loss, migration of osteoclasts, and release of proinflammatory cytokines in maxillae. Anti-TNF-α therapy prevented the development of both AIA and PD. AIA did not modify bacterial counts in the oral cavity. PD, but not AIA, induced by injection of Ag in immunized mice was decreased by local treatment with antiseptic, which decreased the oral microbiota. AIA was associated with an increase in serum C-reactive protein levels and the expression of the transcription factors RORγ and Foxp3 in cervical lymph nodes. There were higher titers of anti-collagen I IgG, and splenocytes were more responsive to collagen I in AIA mice. In conclusion, AIA-induced PD was dependent on TNF-α and the oral microbiota. Moreover, PD was associated with changes in expression of lymphocyte transcription factors, presence of anti-collagen Abs, and increased reactivity to autoantigens.


Assuntos
Artrite Experimental/complicações , Artrite Reumatoide/complicações , Boca/microbiologia , Doenças Periodontais/complicações , Fator de Necrose Tumoral alfa/metabolismo , Animais , Artrite Experimental/imunologia , Artrite Experimental/metabolismo , Artrite Reumatoide/imunologia , Artrite Reumatoide/metabolismo , Ensaio de Imunoadsorção Enzimática , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Doenças Periodontais/imunologia , Doenças Periodontais/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa
9.
Arq Neuropsiquiatr ; 69(6): 938-42, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22297884

RESUMO

Multiple sclerosis is a neuroinflammatory disease that results in serious neurological disability. Besides physical impairment, behavioral symptoms are also common in patients with multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is considered to be a model of multiple sclerosis and mimics the main features of the disease, such as demyelination and motor impairment. In this work, we aimed to study behavioral parameters in animals with EAE using the MOG(35-55) model in C57BL/6 mice. We analyzed memory and anxiety in animals using the elevated plus maze, the step down inhibitory avoidance task and the memory recognition test. No differences in any tests were found when comparing controls and animals induced with EAE. Therefore, we conclude that behavioral changes in animals with EAE induced with MOG(35-55) are probably subtle or absent.


Assuntos
Ansiedade/psicologia , Comportamento Animal/fisiologia , Modelos Animais de Doenças , Encefalomielite Autoimune Experimental/psicologia , Memória/fisiologia , Animais , Ansiedade/fisiopatologia , Aprendizagem da Esquiva/fisiologia , Encefalomielite Autoimune Experimental/fisiopatologia , Feminino , Aprendizagem em Labirinto/fisiologia , Camundongos , Camundongos Endogâmicos C57BL
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