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[PMID]:27632561
[Au] Autor:Rastad JL; Green WR
[Ad] Endereço:Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH 03756, United States.
[Ti] Título:Myeloid-derived suppressor cells in murine AIDS inhibit B-cell responses in part via soluble mediators including reactive oxygen and nitrogen species, and TGF-ß.
[So] Source:Virology;499:9-22, 2016 Dec.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Monocytic myeloid-derived suppressor cells (M-MDSCs) were increased during LP-BM5 retroviral infection, and were capable of suppressing not only T-cell, but also B-cell responses. In addition to previously demonstrating iNOS- and VISTA-dependent M-MDSC mechanisms, in this paper, we detail how M-MDSCs utilized soluble mediators, including the reactive oxygen and nitrogen species superoxide, peroxynitrite, and nitric oxide, and TGF-ß, to suppress B cells in a predominantly contact-independent manner. Suppression was independent of cysteine-depletion and hydrogen peroxide production. When two major mechanisms of suppression (iNOS and VISTA) were eliminated in double knockout mice, M-MDSCs from LP-BM5-infected mice were able to compensate using other, soluble mechanisms in order to maintain suppression of B cells. The IL-10 producing regulatory B-cell compartment was among the targets of M-MDSC-mediated suppression.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Linfócitos B/metabolismo
Síndrome de Imunodeficiência Adquirida Murina/imunologia
Síndrome de Imunodeficiência Adquirida Murina/metabolismo
Células Supressoras Mieloides/imunologia
Células Supressoras Mieloides/metabolismo
Espécies Reativas de Nitrogênio
Espécies Reativas de Oxigênio
Fator de Crescimento Transformador beta/sangue
[Mh] Termos MeSH secundário: Animais
Linfócitos B Reguladores/imunologia
Linfócitos B Reguladores/metabolismo
Comunicação Celular
Tolerância Imunológica
Masculino
Camundongos
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Ácido Peroxinitroso/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Nitrogen Species); 0 (Reactive Oxygen Species); 0 (Transforming Growth Factor beta); 14691-52-2 (Peroxynitrous Acid); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE


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[PMID]:27226373
[Au] Autor:Brundu S; Palma L; Picceri GG; Ligi D; Orlandi C; Galluzzi L; Chiarantini L; Casabianca A; Schiavano GF; Santi M; Mannello F; Green K; Smietana M; Magnani M; Fraternale A
[Ad] Endereço:Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, PU, Italy.
[Ti] Título:Glutathione Depletion Is Linked with Th2 Polarization in Mice with a Retrovirus-Induced Immunodeficiency Syndrome, Murine AIDS: Role of Proglutathione Molecules as Immunotherapeutics.
[So] Source:J Virol;90(16):7118-30, 2016 Aug 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Injection of the LP-BM5 murine leukemia virus into mice causes murine AIDS, a disease characterized by many dysfunctions of immunocompetent cells. To establish whether the disease is characterized by glutathione imbalance, reduced glutathione (GSH) and cysteine were quantified in different organs. A marked redox imbalance, consisting of GSH and/or cysteine depletion, was found in the lymphoid organs, such as the spleen and lymph nodes. Moreover, a significant decrease in cysteine and GSH levels in the pancreas and brain, respectively, was measured at 5 weeks postinfection. The Th2 immune response was predominant at all times investigated, as revealed by the expression of Th1/Th2 cytokines. Furthermore, investigation of the activation status of peritoneal macrophages showed that the expression of genetic markers of alternative activation, namely, Fizz1, Ym1, and Arginase1, was induced. Conversely, expression of inducible nitric oxide synthase, a marker of classical activation of macrophages, was detected only when Th1 cytokines were expressed at high levels. In vitro studies revealed that during the very early phases of infection, GSH depletion and the downregulation of interleukin-12 (IL-12) p40 mRNA were correlated with the dose of LP-BM5 used to infect the macrophages. Treatment of LP-BM5-infected mice with N-(N-acetyl-l-cysteinyl)-S-acetylcysteamine (I-152), an N-acetyl-cysteine supplier, restored GSH/cysteine levels in the organs, reduced the expression of alternatively activated macrophage markers, and increased the level of gamma interferon production, while it decreased the levels of Th2 cytokines, such as IL-4 and IL-5. Our findings thus establish a link between GSH deficiency and Th1/Th2 disequilibrium in LP-BM5 infection and indicate that I-152 can be used to restore the GSH level and a balanced Th1/Th2 response in infected mice. IMPORTANCE: The first report of an association between Th2 polarization and alteration of the redox state in LP-BM5 infection is presented. Moreover, it provides evidence that LP-BM5 infection causes a decrease in the thiol content of peritoneal macrophages, which can influence IL-12 production. The restoration of GSH levels by GSH-replenishing molecules can represent a new therapeutic avenue to fight this retroviral infection, as it reestablishes the Th1/Th2 balance. Immunotherapy based on the use of pro-GSH molecules would permit LP-BM5 infection and probably all those viral infections characterized by GSH deficiency and a Th1/Th2 imbalance to be more effectively combated.
[Mh] Termos MeSH primário: Glutationa/deficiência
Vírus da Leucemia Murina/patogenicidade
Leucemia Experimental/complicações
Síndrome de Imunodeficiência Adquirida Murina/etiologia
Infecções por Retroviridae/complicações
Células Th2/imunologia
Infecções Tumorais por Vírus/complicações
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Citocinas/metabolismo
Feminino
Leucemia Experimental/imunologia
Leucemia Experimental/virologia
Ativação Linfocitária
Macrófagos Peritoneais/imunologia
Macrófagos Peritoneais/metabolismo
Macrófagos Peritoneais/virologia
Camundongos
Camundongos Endogâmicos C57BL
Síndrome de Imunodeficiência Adquirida Murina/metabolismo
Síndrome de Imunodeficiência Adquirida Murina/patologia
Infecções por Retroviridae/imunologia
Infecções por Retroviridae/virologia
Baço/imunologia
Baço/metabolismo
Baço/virologia
Células Th1/imunologia
Células Th1/metabolismo
Células Th1/virologia
Células Th2/metabolismo
Células Th2/virologia
Infecções Tumorais por Vírus/imunologia
Infecções Tumorais por Vírus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160527
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.00603-16


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[PMID]:26076116
[Au] Autor:Kim OK; Nam DE; Yoon HG; Baek SJ; Jun W; Lee J
[Ad] Endereço:1 Department of Medical Nutrition, Kyung Hee University , Yongin, Korea.
[Ti] Título:Immunomodulatory and Antioxidant Effects of Purple Sweet Potato Extract in LP-BM5 Murine Leukemia Virus-Induced Murine Acquired Immune Deficiency Syndrome.
[So] Source:J Med Food;18(8):882-9, 2015 Aug.
[Is] ISSN:1557-7600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The immunomodulatory effects of a dietary supplement of purple sweet potato extract (PSPE) in LP-BM5 murine leukemia virus (MuLV)-induced immune-deficient mice were investigated. Mice were divided into six groups: normal control, infected control (LP-BM5 MuLV infection), positive control (LP-BM5 MuLV infection+dietary supplement of red ginseng 300 mg/kg), purple sweet potato water extract (PSPWE) (LP-BM5 MuLV infection+dietary supplement of PSPE 300 mg/kg), PSP10EE (LP-BM5 MuLV infection+dietary supplement of 10% ethanol PSPE 300 mg/kg), and PSP80EE (LP-BM5 MuLV infection+dietary supplement of 80% ethanol PSPE 300 mg/kg). Dietary supplementation began on the day of LP-BM5 MuLV infection and continued for 12 weeks. Dietary supplementation of PSPE inhibited LP-BM5 MuLV-induced splenomegaly and lymphadenopathy and attenuated the suppression of T- and B-cell proliferation and T helper 1/T helper 2 cytokine imbalance in LP-BM5 MuLV-infected mice. Dietary supplement of PSPE increased the activity of the antioxidant enzymes, superoxide dismutase and glutathione peroxidase. The data suggest that PSPE may ameliorate immune dysfunction due to LP-BM5 MuLV infection by modulating antioxidant defense systems.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Imunomodulação/efeitos dos fármacos
Ipomoea batatas/química
Ipomoea batatas/imunologia
Vírus da Leucemia Murina
Síndrome de Imunodeficiência Adquirida Murina/dietoterapia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/química
Linfócitos B/citologia
Linfócitos B/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Citocinas/análise
Modelos Animais de Doenças
Glutationa Peroxidase/metabolismo
Vírus da Leucemia Murina/patogenicidade
Doenças Linfáticas/dietoterapia
Camundongos
Camundongos Endogâmicos C57BL
Síndrome de Imunodeficiência Adquirida Murina/imunologia
Síndrome de Imunodeficiência Adquirida Murina/patologia
Síndrome de Imunodeficiência Adquirida Murina/virologia
Extratos Vegetais/farmacologia
Preparações de Plantas/química
Esplenomegalia/dietoterapia
Superóxido Dismutase/metabolismo
Linfócitos T/citologia
Linfócitos T/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cytokines); 0 (Plant Extracts); 0 (Plant Preparations); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:150728
[Lr] Data última revisão:
150728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150616
[St] Status:MEDLINE
[do] DOI:10.1089/jmf.2014.3274


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[PMID]:24629894
[Au] Autor:McLane VD; Cao L; Willis CL
[Ad] Endereço:Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME 04473, USA; Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME 04005, USA; Center for Excellence in the Neurosciences, University of New England, Biddeford, ME 04005, USA. Electronic address: vdmclane@gmail.com.
[Ti] Título:Morphine increases hippocampal viral load and suppresses frontal lobe CCL5 expression in the LP-BM5 AIDS model.
[So] Source:J Neuroimmunol;269(1-2):44-51, 2014 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic opiate abuse accelerates the development of cognitive deficits in human immunodeficiency virus (HIV)-1 patients. To investigate morphine's effects on viral infection of the central nervous system, we applied chronic morphine treatment to the LP-BM5 murine acquired immunodeficiency syndrome (MAIDS) model. LP-BM5 infection induces proinflammatory cytokine/chemokine production, correlating to increased blood-brain barrier permeability. Morphine treatment significantly increased LP-BM5 viral load in the hippocampus, but not in the frontal lobe. Morphine reduced the chemokine CCL5 to non-infected levels in the frontal lobe, but not in the hippocampus. These data indicate a region-specific mechanism for morphine's effects on virally-induced neurocognitive deficits.
[Mh] Termos MeSH primário: Quimiocina CCL5/biossíntese
Lobo Frontal/metabolismo
Hipocampo/metabolismo
Morfina/toxicidade
Síndrome de Imunodeficiência Adquirida Murina/metabolismo
Carga Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Síndrome de Imunodeficiência Adquirida/metabolismo
Animais
Quimiocina CCL5/antagonistas & inibidores
Lobo Frontal/efeitos dos fármacos
Lobo Frontal/virologia
Regulação da Expressão Gênica
Hipocampo/efeitos dos fármacos
Hipocampo/virologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Carga Viral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ccl5 protein, mouse); 0 (Chemokine CCL5); 76I7G6D29C (Morphine)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140318
[St] Status:MEDLINE


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[PMID]:24335302
[Au] Autor:O'Connor MA; Green WR
[Ad] Endereço:Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
[Ti] Título:Use of IRF-3 and/or IRF-7 knockout mice to study viral pathogenesis: lessons from a murine retrovirus-induced AIDS model.
[So] Source:J Virol;88(4):2349-53, 2014 Feb.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interferon regulatory factor (IRF) regulation of the type I interferon response has not been extensively explored in murine retroviral infections. IRF-3(-/-) and select IRF-3/7(-/-) mice were resistant to LP-BM5-induced pathogenesis. However, further analyses strongly suggested that resistance could be attributed to strain 129-specific contamination of the known retrovirus resistance gene Fv1. Therefore, caution should be taken when interpreting phenotypes observed in these knockout mice, as strain 129-derived genetic polymorphisms may explain observed differences.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Gammaretrovirus/imunologia
Fator Regulador 3 de Interferon/genética
Fator Regulador 7 de Interferon/genética
Interferon Tipo I/imunologia
Síndrome de Imunodeficiência Adquirida Murina/imunologia
Síndrome de Imunodeficiência Adquirida Murina/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Eletroforese
Gammaretrovirus/genética
Camundongos
Camundongos Knockout
Síndrome de Imunodeficiência Adquirida Murina/virologia
Proteínas/genética
Proteínas/imunologia
Especificidade da Espécie
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fv1 protein, mouse); 0 (Interferon Regulatory Factor-3); 0 (Interferon Regulatory Factor-7); 0 (Interferon Type I); 0 (Proteins)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131217
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.02960-13


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[PMID]:23902750
[Au] Autor:Mutnal MB; Schachtele SJ; Hu S; Lokensgard JR
[Ad] Endereço:Neuroimmunology Laboratory, Center for Infectious Diseases and Microbiology Translational Research, Department of Medicine, University of Minnesota, 3-220 LRB/MTRF, 2001 6th Street S.E., Minneapolis, MN 55455, USA.
[Ti] Título:T-cell reconstitution during murine acquired immunodeficiency syndrome (MAIDS) produces neuroinflammation and mortality in animals harboring opportunistic viral brain infection.
[So] Source:J Neuroinflammation;10:98, 2013 Jul 31.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Highly active antiretroviral therapy (HAART) restores inflammatory immune responses in AIDS patients which may unmask previous subclinical infections or paradoxically exacerbate symptoms of opportunistic infections. In resource-poor settings, 25% of patients receiving HAART may develop CNS-related immune reconstitution inflammatory syndrome (IRIS). Here we describe a reliable mouse model to study underlying immunopathological mechanisms of CNS-IRIS. METHODS: Utilizing our HSV brain infection model and mice with MAIDS, we investigated the effect of immune reconstitution on MAIDS mice harboring opportunistic viral brain infection. Using multi-color flow cytometry, we quantitatively measured the cellular infiltrate and microglial activation. RESULTS: Infection with the LP-BM5 retroviral mixture was found to confer susceptibility to herpes simplex virus (HSV)-1 brain infection to normally-resistant C57BL/6 mice. Increased susceptibility to brain infection was due to severe immunodeficiency at 8 wks p.i. and a marked increase in programmed death-1 (PD-1) expression on CD4+ and CD8+ T-cells. Both T-cell loss and opportunistic brain infection were associated with high level PD-1 expression because PD-1-knockout mice infected with LP-BM5 did not exhibit lymphopenia and retained resistance to HSV-1. In addition, HSV-infection of MAIDS mice stimulated peripheral immune cell infiltration into the brain and its ensuing microglial activation. Interestingly, while opportunistic herpes virus brain infection of C57BL/6 MAIDS mice was not itself lethal, when T-cell immunity was reconstituted through adoptive transfer of virus-specific CD3+ T-cells, it resulted in significant mortality among recipients. This immune reconstitution-induced mortality was associated with exacerbated neuroinflammation, as determined by MHC class II expression on resident microglia and elevated levels of Th1 cytokines in the brain. CONCLUSIONS: Taken together, these results indicate development of an immune reconstitution disease within the central nervous system (CNS-IRD). Experimental immune reconstitution disease of the CNS using T-cell repopulation of lymphopenic murine hosts harboring opportunistic brain infections may help elucidate neuroimmunoregulatory networks that produce CNS-IRIS in patients initiating HAART.
[Mh] Termos MeSH primário: Infecções Oportunistas Relacionadas com a AIDS/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Viroses do Sistema Nervoso Central/imunologia
Herpes Simples/imunologia
Síndrome de Imunodeficiência Adquirida Murina/imunologia
[Mh] Termos MeSH secundário: Infecções Oportunistas Relacionadas com a AIDS/mortalidade
Infecções Oportunistas Relacionadas com a AIDS/patologia
Animais
Linfócitos T CD4-Positivos/patologia
Linfócitos T CD4-Positivos/virologia
Linfócitos T CD8-Positivos/patologia
Linfócitos T CD8-Positivos/virologia
Viroses do Sistema Nervoso Central/mortalidade
Viroses do Sistema Nervoso Central/patologia
Herpes Simples/mortalidade
Herpes Simples/patologia
Inflamação/imunologia
Inflamação/mortalidade
Inflamação/patologia
Camundongos
Camundongos Endogâmicos C57BL
Síndrome de Imunodeficiência Adquirida Murina/mortalidade
Síndrome de Imunodeficiência Adquirida Murina/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1403
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130802
[St] Status:MEDLINE
[do] DOI:10.1186/1742-2094-10-98


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[PMID]:23726765
[Au] Autor:Cao L; Butler MB
[Ad] Endereço:Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, 11 Hills Beach Road, Biddeford, ME 04005, USA. lcao@UNE.edu
[Ti] Título:Involvement of microglial CD40 in murine retrovirus-induced peripheral neuropathy.
[So] Source:J Neuroimmunol;261(1-2):37-43, 2013 Aug 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:B6 mice infected with LP-BM5 develop severe immunodeficiency (termed murine acquired immunodeficiency syndrome (MAIDS)) and peripheral neuropathy. To determine whether microglial CD40 is involved in LP-BM5-induced peripheral neuropathy, B6-CD40 knockout (KO) mice and B6-CD40 KO mice adoptively transferred either total leukocytes or B cells were examined for behavioral sensitivity, tissue viral loads, cytokine responses, and the development of MAIDS. All three CD40 KO groups developed MAIDS, the severity of which was correlated with peripheral cytokine responses. CD40 KO mice displayed significantly reduced mechanical hypersensitivity post-infection compared to wild-type mice regardless of cell transfer. These findings support microglial CD40 involvement in LP-BM5-induced peripheral neuropathy.
[Mh] Termos MeSH primário: Antígenos CD40/imunologia
Vírus da Leucemia Murina/imunologia
Microglia/imunologia
Síndrome de Imunodeficiência Adquirida Murina/imunologia
Doenças do Sistema Nervoso Periférico/metabolismo
Retroviridae/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Linfócitos B/patologia
Linfócitos B/virologia
Antígenos CD40/deficiência
Leucócitos/imunologia
Leucócitos/patologia
Leucócitos/virologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microglia/patologia
Microglia/virologia
Síndrome de Imunodeficiência Adquirida Murina/patologia
Síndrome de Imunodeficiência Adquirida Murina/virologia
Doenças do Sistema Nervoso Periférico/imunologia
Doenças do Sistema Nervoso Periférico/virologia
Distribuição Aleatória
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CD40 Antigens)
[Em] Mês de entrada:1310
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130604
[St] Status:MEDLINE


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[PMID]:23680027
[Au] Autor:O'Connor MA; Green WR
[Ad] Endereço:Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire 03756, USA.
[Ti] Título:The role of indoleamine 2,3-dioxygenase in LP-BPM5 murine retroviral disease progression.
[So] Source:Virol J;10:154, 2013 May 17.
[Is] ISSN:1743-422X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Indoleamine 2,3-dioxygenase (IDO) is an immunomodulatory intracellular enzyme involved in tryptophan degradation. IDO is induced during cancer and microbial infections by cytokines, ligation of co-stimulatory molecules and/or activation of pattern recognition receptors, ultimately leading to modulation of the immune response. LP-BM5 murine retroviral infection induces murine AIDS (MAIDS), which is characterized by profound and broad immunosuppression of T- and B-cell responses. Our lab has previously described multiple mechanisms regulating the development of immunodeficiency of LP-BM5-induced disease, including Programmed Death 1 (PD-1), IL-10, and T-regulatory (Treg) cells. Immunosuppressive roles of IDO have been demonstrated in other retroviral models, suggesting a possible role for IDO during LP-BM5-induced retroviral disease progression and/or development of viral load. METHODS: Mice deficient in IDO (B6.IDO-/-) and wildtype C57BL/6 (B6) mice were infected with LP-BM5 murine retrovirus. MAIDS and LP-BM5 viral load were assessed at termination. RESULTS: As expected, IDO was un-inducible in B6.IDO-/- during LP-BM5 infection. B6.IDO-/- mice infected with LP-BM5 retrovirus succumbed to MAIDS as indicated by splenomegaly, serum hyper IgG2a and IgM, decreased responsiveness to B- and T-cell mitogens, conversion of a proportion of CD4+ T cells from Thy1.2+ to Thy1.2-, and increased percentages of CD11b+Gr-1+ cells. LP-BM5 infected B6.IDO-/- mice also demonstrated the development of roughly equivalent disease kinetics as compared to infected B6 mice. Splenic viral loads of B6 and B6.IDO-/- mice were also equivalent after infection as measured by LP-BM5-specific Def Gag and Eco Gag viral mRNA, determined by qRT-PCR. CONCLUSIONS: Collectively, these results demonstrate IDO neither plays an essential role, nor is required, in LP-BM5-induced disease progression or LP-BM5 viral load.
[Mh] Termos MeSH primário: Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Síndrome de Imunodeficiência Adquirida Murina/patologia
Retroviridae/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Progressão da Doença
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Indoleamine-Pyrrole 2,3,-Dioxygenase)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130518
[St] Status:MEDLINE
[do] DOI:10.1186/1743-422X-10-154


  9 / 435 MEDLINE  
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[PMID]:23415673
[Au] Autor:Blalock EL; Chien H; Dix RD
[Ad] Endereço:Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, GA 30303, United States.
[Ti] Título:Murine cytomegalovirus downregulates interleukin-17 in mice with retrovirus-induced immunosuppression that are susceptible to experimental cytomegalovirus retinitis.
[So] Source:Cytokine;61(3):862-75, 2013 Mar.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Interleukin-17 (IL-17), a pro-inflammatory cytokine produced by CD4+ Th17 cells, has been associated with the pathogenesis of several autoimmune diseases including uveitis. The fate of IL-17 during HIV/AIDS, however, remains unclear, and a possible role for IL-17 in the pathogenesis of AIDS-related diseases has not been investigated. Toward these ends, we performed studies using a well-established animal model of experimental murine cytomegalovirus (MCMV) retinitis that develops in C57/BL6 mice with retrovirus-induced immunosuppression (MAIDS). After establishing baseline levels for IL-17 production in whole splenic cells of healthy mice, we observed a significant increase in IL-17 mRNA levels in whole splenic cells of mice with MAIDS of 4-weeks (MAIDS-4), 8-weeks (MAIDS-8), and 10-weeks (MAIDS-10) duration. In contrast, enriched populations of splenic CD4+ T cells, splenic macrophages, and splenic neutrophils exhibited a reproducible decrease in levels of IL-17 mRNA during MAIDS progression. To explore a possible role for IL-17 during the pathogenesis of MAIDS-related MCMV retinitis, we first demonstrated constitutive IL-17 expression in retinal photoreceptor cells of uninfected eyes of healthy mice. Subsequent studies, however, revealed a significant decrease in intraocular levels of IL-17 mRNA and protein in MCMV-infected eyes of MAIDS-10 mice during retinitis development. That MCMV infection might cause a remarkable downregulation of IL-17 production was supported further by the finding that systemic MCMV infection of healthy, MAIDS-4, or MAIDS-10 mice also significantly decreased IL-17 mRNA production by splenic CD4+ T cells. Based on additional studies using IL-10 -/- mice infected systemically with MCMV and IL-10 -/- mice with MAIDS infected intraocularly with MCMV, we propose that MCMV infection downregulates IL-17 production via stimulation of suppressor of cytokine signaling (SOCS)-3 and interleukin-10.
[Mh] Termos MeSH primário: Retinite por Citomegalovirus/patologia
Retinite por Citomegalovirus/virologia
Regulação para Baixo
Interleucina-17/metabolismo
Síndrome de Imunodeficiência Adquirida Murina/imunologia
Síndrome de Imunodeficiência Adquirida Murina/virologia
Muromegalovirus/fisiologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/metabolismo
Retinite por Citomegalovirus/genética
Retinite por Citomegalovirus/imunologia
Progressão da Doença
Suscetibilidade a Doenças
Olho/metabolismo
Feminino
Imunossupressão
Interleucina-17/biossíntese
Interleucina-17/genética
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Síndrome de Imunodeficiência Adquirida Murina/genética
Síndrome de Imunodeficiência Adquirida Murina/patologia
Neutrófilos/metabolismo
Células Fotorreceptoras de Vertebrados/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Retroviridae/fisiologia
Baço/metabolismo
Baço/patologia
Proteína 1 Supressora da Sinalização de Citocina
Proteína 3 Supressora da Sinalização de Citocinas
Proteínas Supressoras da Sinalização de Citocinas/genética
Proteínas Supressoras da Sinalização de Citocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-17); 0 (RNA, Messenger); 0 (Socs1 protein, mouse); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 1 Protein); 0 (Suppressor of Cytokine Signaling 3 Protein); 0 (Suppressor of Cytokine Signaling Proteins)
[Em] Mês de entrada:1308
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130219
[St] Status:MEDLINE


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[PMID]:22956581
[Au] Autor:Cao L; Butler MB; Tan L; Draleau KS; Koh WY
[Ad] Endereço:Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME 04005, USA. lcao@UNE.edu
[Ti] Título:Murine immunodeficiency virus-induced peripheral neuropathy and the associated cytokine responses.
[So] Source:J Immunol;189(7):3724-33, 2012 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Distal symmetrical polyneuropathy is the most common form of HIV infection-associated peripheral neuropathy and is often associated with pain. C57BL/6 (B6) mice infected with LP-BM5, a murine retroviral isolate, develop a severe immunodeficiency syndrome similar to that in humans infected with HIV-1, hence the term murine AIDS. We investigated the induction of peripheral neuropathy after LP-BM5 infection in B6 mice. Infected B6 mice, like HIV-infected humans, exhibited behavioral (increased sensitivity to mechanical and heat stimuli) and pathological (transient loss of intraepidermal nerve fibers) signs of peripheral neuropathy. The levels of viral gag RNA were significantly increased in all tissues tested, including spleen, paw skin, lumbar dorsal root ganglia, and lumbar spinal cord, postinfection (p.i.). Correlated with the development of peripheral neuropathy, the tissue levels of several cytokines, including IFN-γ, IL-1ß, IL-6, and IL-12, were significantly elevated p.i. These increases had cytokine-specific and tissue-specific profiles and kinetics. Further, treatment with the antiretroviral agent zidovudine either significantly reduced or completely reversed the aforementioned behavioral, pathologic, and cytokine changes p.i. These data suggest that LP-BM5 infection is a potential mouse model of HIV-associated distal symmetrical polyneuropathy that can be used for investigating the roles of various cytokines in infection-induced neuropathic pain. Further investigation of this model could give a better understanding of, and lead to more effective treatments for, HIV infection-associated painful peripheral neuropathy.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Vírus da Leucemia Murina/imunologia
Síndrome de Imunodeficiência Adquirida Murina/imunologia
Síndrome de Imunodeficiência Adquirida Murina/metabolismo
Doenças do Sistema Nervoso Periférico/imunologia
Doenças do Sistema Nervoso Periférico/virologia
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Modelos Animais de Doenças
Hipersensibilidade/imunologia
Hipersensibilidade/metabolismo
Hipersensibilidade/virologia
Vírus da Leucemia Murina/isolamento & purificação
Leucemia Experimental/imunologia
Leucemia Experimental/metabolismo
Leucemia Experimental/virologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Doenças do Sistema Nervoso Periférico/metabolismo
RNA Mensageiro/biossíntese
Infecções por Retroviridae/imunologia
Infecções por Retroviridae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cytokines); 0 (RNA, Messenger)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120908
[St] Status:MEDLINE



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