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  1 / 1897 MEDLINE  
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[PMID]:29363152
[Au] Autor:Rodrigues Oliveira JL; Teixeira MM; Lambertucci JR; Antunes CMF; Carneiro M; Negrão-Corrêa D
[Ad] Endereço:Departamento de Parasitologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Título:Plasma levels of innate immune mediators are associated with liver fibrosis in low parasite burden Schistosoma mansoni-infected individuals.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the murine model, it was demonstrated that pro-inflammatory cytokines and chemokines are essential to the formation and modulation of Schistosoma-induced granulomatous inflammation. However, the relationship of these immune mediators and disease severity is hard to be established in naturally infected individuals. The current study evaluates the association between plasma concentrations of MIF, sTNF-R1, CCL3, CCL7 and CCL24 and schistosomiasis morbidity in Schistosoma mansoni-infected patients with a low parasite burden. For this propose, 97 S. mansoni-infected individuals were subjected to abdominal ultrasound analysis and clinical examination. Among them, 88 had plasma concentration of immune mediators estimated by ELISA assay. Multivariate linear regression models were used to evaluate the relationship between the plasma concentration of immune mediators and the variables investigated. Although most individuals presented low parasite burden, over 30% of them showed signs of fibrosis defined by ultrasound measurements and 2 patients had a severe form of schistosomiasis. No association between parasite burden and the plasma levels of chemokine/cytokines or disease severity was observed. There was a positive association between plasma concentration of CCL4, sTNF-R1, CCL3 and MIF with gall bladder thickness and/or with portal vein thickness that are liver fibrosis markers. In contrast, no association was found between CCL7 plasma concentrations with any of the schistosomiasis morbidity parameters evaluated. The data showed that CCL24, sTNFR1, MIF and CCL3 can be detected in plasma of S. mansoni-infected individuals and their concentration would be used as prognostic makers of Schistosoma-induced liver fibrosis, even in individuals with low parasite burden.
[Mh] Termos MeSH primário: Quimiocina CCL24/sangue
Quimiocina CCL3/sangue
Quimiocina CCL7/sangue
Oxirredutases Intramoleculares/sangue
Cirrose Hepática/imunologia
Fatores Inibidores da Migração de Macrófagos/sangue
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
Schistosoma mansoni/imunologia
Esquistossomose mansoni/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Animais
Seres Humanos
Fígado/irrigação sanguínea
Fígado/parasitologia
Fígado/patologia
Cirrose Hepática/parasitologia
Meia-Idade
Veia Porta/patologia
Esquistossomose mansoni/parasitologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL24 protein, human); 0 (CCL3 protein, human); 0 (CCL7 protein, human); 0 (Chemokine CCL24); 0 (Chemokine CCL3); 0 (Chemokine CCL7); 0 (Macrophage Migration-Inhibitory Factors); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (TNFRSF1A protein, human); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (MIF protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12642


  2 / 1897 MEDLINE  
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[PMID]:28847849
[Au] Autor:Deniffel D; Nuyen B; Pak K; Suzukawa K; Hung J; Kurabi A; Wasserman SI; Ryan AF
[Ad] Endereço:Department of Surgery/Otolaryngology, University of California, San Diego, La Jolla, California, USA.
[Ti] Título:Otitis Media and Nasopharyngeal Colonization in Mice.
[So] Source:Infect Immun;85(11), 2017 Nov.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously found CC chemokine ligand 3 (CCL3) to be a potent effector of inflammation during otitis media (OM): exogenous CCL3 rescues the OM phenotype of tumor necrosis factor-deficient mice and the function of macrophages deficient in several innate immune molecules. To further delineate the role of CCL3 in OM, we evaluated middle ear (ME) responses of mice to nontypeable (NTHi). CCL chemokine gene expression was evaluated in wild-type (WT) mice during the complete course of acute OM. OM was induced in and WT mice, and infection and inflammation were monitored for 21 days. Phagocytosis and killing of NTHi by macrophages were evaluated by an assay. The nasopharyngeal bacterial load was assessed in naive animals of both strains. Many CCL genes showed increased expression levels during acute OM, with CCL3 being the most upregulated, at levels 600-fold higher than the baseline. deletion compromised ME bacterial clearance and prolonged mucosal hyperplasia. ME recruitment of leukocytes was delayed but persisted far longer than in WT mice. These events were linked to a decrease in the macrophage capacity for NTHi phagocytosis and increased nasopharyngeal bacterial loads in mice. The generalized impairment in inflammatory cell recruitment was associated with compensatory changes in the expression profiles of CCL2, CCL7, and CCL12. CCL3 plays a significant role in the clearance of infection and resolution of inflammation and contributes to mucosal host defense of the nasopharyngeal niche, a reservoir for ME and upper respiratory infections. Therapies based on CCL3 could prove useful in treating or preventing persistent disease.
[Mh] Termos MeSH primário: Quimiocina CCL3/imunologia
Orelha Média/imunologia
Infecções por Haemophilus/imunologia
Haemophilus influenzae/imunologia
Nasofaringe/imunologia
Otite Média/imunologia
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Movimento Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CCL3/deficiência
Quimiocina CCL3/genética
Quimiocina CCL7/genética
Quimiocina CCL7/imunologia
Modelos Animais de Doenças
Orelha Média/microbiologia
Regulação da Expressão Gênica
Infecções por Haemophilus/genética
Infecções por Haemophilus/microbiologia
Infecções por Haemophilus/patologia
Interações Hospedeiro-Patógeno
Leucócitos/imunologia
Leucócitos/microbiologia
Macrófagos/imunologia
Macrófagos/microbiologia
Camundongos
Camundongos Knockout
Proteínas Quimioatraentes de Monócitos/genética
Proteínas Quimioatraentes de Monócitos/imunologia
Nasofaringe/microbiologia
Otite Média/genética
Otite Média/microbiologia
Otite Média/patologia
Fagocitose
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl12 protein, mouse); 0 (Ccl2 protein, mouse); 0 (Ccl3 protein, mouse); 0 (Ccl7 protein, mouse); 0 (Chemokine CCL2); 0 (Chemokine CCL3); 0 (Chemokine CCL7); 0 (Monocyte Chemoattractant Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE


  3 / 1897 MEDLINE  
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[PMID]:28750923
[Au] Autor:Caslin HL; McLeod JJA; Spence AJ; Qayum AA; Kolawole EM; Taruselli MT; Paranjape A; Elford HL; Ryan JJ
[Ad] Endereço:Department of Biology, Virginia Commonwealth University, Richmond, VA, 23284, United States.
[Ti] Título:Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IL-33-induced cytokine production in primary mouse mast cells.
[So] Source:Cell Immunol;319:10-16, 2017 Sep.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:While IgE is considered the primary mediator of mast cell activation, IL-33 contributes substantially in asthma, allergic rhinitis, and atopic dermatitis. To develop effective treatments for allergic disease, it is important to understand the role of therapeutic agents on IL-33 activation. We examined the effect of Didox (3,4-dihydroxybenzohydroxamic acid), an antioxidant and ribonucleotide reductase (RNR) inhibitor, on IL-33-mediated mast cell activation. Didox suppressed IL-6, IL-13, TNF, and MIP-1α (CCL3) production in bone marrow derived mast cells following IL-33 activation. This suppression was observed in different genetic backgrounds and extended to peritoneal mast cells. The antioxidant N-acetylcysteine mimicked the suppression of Didox, albeit at a much higher dose, while the RNR inhibitor hydroxyurea had no effect. Didox substantially suppressed IL-33-mediated NFκB and AP-1 transcriptional activities. These results suggest that Didox attenuates IL-33-induced mast cell activation and should be further studied as a potential therapeutic agent for inflammatory diseases involving IL-33.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/efeitos dos fármacos
Ácidos Hidroxâmicos/farmacologia
Imunossupressores/farmacologia
Interleucina-33/farmacologia
Mastócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Animais
Células da Medula Óssea/citologia
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Quimiocina CCL3/antagonistas & inibidores
Quimiocina CCL3/genética
Quimiocina CCL3/imunologia
Feminino
Regulação da Expressão Gênica/imunologia
Genes Reporter
Hidroxiureia/farmacologia
Interleucina-13/antagonistas & inibidores
Interleucina-13/genética
Interleucina-13/imunologia
Interleucina-33/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Luciferases/genética
Luciferases/imunologia
Masculino
Mastócitos/citologia
Mastócitos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/antagonistas & inibidores
NF-kappa B/genética
NF-kappa B/imunologia
Cultura Primária de Células
Transdução de Sinais
Fator de Transcrição AP-1/antagonistas & inibidores
Fator de Transcrição AP-1/genética
Fator de Transcrição AP-1/imunologia
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl3 protein, mouse); 0 (Chemokine CCL3); 0 (Hydroxamic Acids); 0 (Il33 protein, mouse); 0 (Immunosuppressive Agents); 0 (Interleukin-13); 0 (Interleukin-33); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Transcription Factor AP-1); 0 (Tumor Necrosis Factor-alpha); EC 1.13.12.- (Luciferases); L106XFV0RQ (3,4-dihydroxybenzohydroxamic acid); WYQ7N0BPYC (Acetylcysteine); X6Q56QN5QC (Hydroxyurea)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE


  4 / 1897 MEDLINE  
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[PMID]:28633455
[Au] Autor:Schoeman JC; Moutloatse GP; Harms AC; Vreeken RJ; Scherpbier HJ; Van Leeuwen L; Kuijpers TW; Reinecke CJ; Berger R; Hankemeier T; Bunders MJ
[Ad] Endereço:Department of Analytical Biosciences, Leiden Academic Center for Drug Research, Leiden University, The Netherlands.
[Ti] Título:Fetal Metabolic Stress Disrupts Immune Homeostasis and Induces Proinflammatory Responses in Human Immunodeficiency Virus Type 1- and Combination Antiretroviral Therapy-Exposed Infants.
[So] Source:J Infect Dis;216(4):436-446, 2017 Aug 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased morbidity and fetal growth restriction are reported in uninfected children born to human immunodeficiency virus type 1 (HIV-1)-infected women treated with antiretroviral (ARV) therapy. Viruses and/or pharmacological interventions such as ARVs can induce metabolic stress, skewing the cell's immune response and restricting (cell) growth. Novel metabolomic techniques provided the opportunity to investigate the impact of fetal HIV-1 and combination ARV therapy (cART) exposure on the infants' immune metabolome. Peroxidized lipids, generated by reactive oxygen species, were increased in cART/HIV-1-exposed infants, indicating altered mitochondrial functioning. The lipid metabolism was further dysregulated with increased triglyceride species and a subsequent decrease in phospholipids in cART/HIV-1-exposed infants compared to control infants. Proinflammatory immune mediators, lysophospholipids as well as cytokines such as CXCL10 and CCL3, were increased whereas anti-inflammatory metabolites from the cytochrome P450 pathway were reduced in cART/HIV-1-exposed infants. Taken together, these data demonstrate that the fetal metabolism is impacted by maternal factors (cART and HIV-1) and skews physiological immune responses toward inflammation in the newborn infant.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/uso terapêutico
Infecções por HIV/tratamento farmacológico
Inflamação/imunologia
Estresse Fisiológico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Quimiocina CCL3/sangue
Quimiocina CXCL10/sangue
Colesterol/sangue
Feminino
Feto/efeitos dos fármacos
Feto/imunologia
Infecções por HIV/transmissão
Homeostase/efeitos dos fármacos
Seres Humanos
Hipertrigliceridemia/sangue
Hipertrigliceridemia/tratamento farmacológico
Lactente
Recém-Nascido
Transmissão Vertical de Doença Infecciosa
Peroxidação de Lipídeos
Masculino
Metabolômica
Estresse Oxidativo/efeitos dos fármacos
Fosfolipídeos/sangue
Gravidez
Complicações Infecciosas na Gravidez/tratamento farmacológico
Complicações Infecciosas na Gravidez/virologia
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (CCL3 protein, human); 0 (CXCL10 protein, human); 0 (Chemokine CCL3); 0 (Chemokine CXCL10); 0 (Phospholipids); 0 (Triglycerides); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix291


  5 / 1897 MEDLINE  
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[PMID]:28606241
[Au] Autor:Chen C; Chen Q; Li L; Yu XJ; Ke JW; He MJ; Zhou HP; Yang WP; Wang WX
[Ad] Endereço:Department of Respiratory Medicine, Children's Hospital in Jiangxi Province, Nanchang 330000, China. jx-cq@163.com.
[Ti] Título:[Effects of recombinant fusion protein interleukin-18 on expression of immune-inflammatory factors in mice infected with Staphylococcus aureus].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(6):705-711, 2017 Jun.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To observe the effects of recombinant fusion protein interleukin (IL)-18 on the expression of immune-inflammatory factors in the mice infected with Staphylococcus aureus (SA), and to investigate the mechanism of action of IL-18 in defense of SA infection in vivo. METHODS: A total of 40 specific pathogen-free female BLAB/c mice were randomly divided into four groups: control, SA infection, immunized, and intervention. A mouse model of SA infection was established by nasal inoculation with SA liquid. The immunized group and the intervention group were intranasally given IL-18 before SA modeling, and then the SA infection group and the intervention group received the nasal inoculation with SA liquid; the control group was treated with phosphate buffered saline instead. The levels of IL-4, interferon (IFN)-γ, tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), IgM in the serum and bronchoalveolar lavage fluid (BALF) of mice were measured by enzyme-linked immunosorbent assay. The expression of macrophage inflammatory protein (MIP)-1α mRNA and MIP-2ß mRNA in the lung tissue of mice were determined by real-time fluorescent quantitative PCR. RESULTS: Compared with the control group, the SA infection group and the immunized group had significantly higher levels of IL-4, G-CSF, and IgM in the serum and BALF and expression of MIP-1α mRNA and MIP-2ß mRNA in the lung tissue (P<0.05); the SA infection group had a significantly lower level of IFN-γ and a significantly higher level of TNF in the serum and BALF (P<0.05); the immunized group had a significantly higher level of IFN-γ in the serum and BALF (P<0.05). Compared with the SA infection group, the intervention group had significantly higher levels of IL-4, IFN-γ, G-CSF, and IgM in the serum and BALF and expression of MIP-1α mRNA in the lung tissue. In contrast, the intervention group showed a significantly lower level of TNF in the serum and BALF and expression of MIP-2ß mRNA in the lung tissue (P<0.05). All the above indicators in the intervention group were significantly higher than those in the control group (P<0.05), except the serum level of IFN-γ. CONCLUSIONS: In the mice infected with SA, the recombinant fusion protein IL-18 by mucosal immunity can affect inflammatory factors in the serum and BALF and the expression of MIP-1α mRNA and MIP-2ß mRNA in the lung tissue to promote the anti-infective immune response and enhance the ability to clear pathogens.
[Mh] Termos MeSH primário: Interleucina-18/uso terapêutico
Proteínas Recombinantes de Fusão/uso terapêutico
Infecções Estafilocócicas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Quimiocina CCL3/análise
Feminino
Fator Estimulador de Colônias de Granulócitos/sangue
Interferon gama/sangue
Interleucina-4/sangue
Camundongos
Camundongos Endogâmicos BALB C
Proteínas Recombinantes de Fusão/farmacologia
Infecções Estafilocócicas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl3 protein, mouse); 0 (Chemokine CCL3); 0 (Interleukin-18); 0 (Recombinant Fusion Proteins); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE


  6 / 1897 MEDLINE  
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[PMID]:28594940
[Au] Autor:Nenasheva T; Nikolaev A; Diykanov D; Sukhanova A; Tcyganov E; Panteleev A; Bocharova I; Serdyuk Y; Nezlin L; Radaeva T; Adrianov N; Rubtsov Y; Lyadova I
[Ad] Endereço:Central Tuberculosis Research Institute, Moscow, Russia.
[Ti] Título:The introduction of mesenchymal stromal cells induces different immunological responses in the lungs of healthy and M. tuberculosis infected mice.
[So] Source:PLoS One;12(6):e0178983, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stromal cells (MSC) have strong immunomodulatory properties and therefore can be used to control inflammation and tissue damage. It was suggested recently that MSC injections can be used to treat multi-drug resistant tuberculosis (TB). However, MSC trafficking and immunomodulatory effects of MSC injections during Mycobacterium tuberculosis (Mtb) infection have not been studied. To address this issue we have analyzed MSC distribution in tissues and local immunological effects of MSC injections in Mtb infected and uninfected mice. After intravenous injection, MSC accumulated preferentially in the lungs where they were located as cell aggregates in the alveolar walls. Immunological analysis of MSC effects included detection of activated, IFN-γ and IL-4 producing CD4+ lymphocytes, the frequency analysis of dendritic cells (CD11c+F4/80) and macrophages (CD11c-F4/80+) located in the lungs, the expression of IA/IE and CD11b molecules by these cells, and evaluation of 23 cytokines/chemokines in lung lysates. In the lungs of uninfected mice, MSC transfer markedly increased the percentage of IFN-γ+ CD4+ lymphocytes and dendritic cells, elevated levels of IA/IE expression by dendritic cells and macrophages, augmented local production of type 2 cytokines (IL-4, IL-5, IL-10) and chemokines (CCL2, CCL3, CCL4, CCL5, CXCL1), and downregulated type 1 and hematopoietic cytokines (IL-12p70, IFN-γ, IL-3, IL-6, GM-CSF). Compared to uninfected mice, Mtb infected mice had statistically higher "background" frequency of activated CD69+ and IFN-γ+ CD4+ lymphocytes and dendritic cells, and higher levels of cytokines in the lungs. The injections of MSC to Mtb infected mice did not show statistically significant effects on CD4+ lymphocytes, dendritic cells and macrophages, only slightly shifted cytokine profile, and did not change pathogen load or slow down TB progression. Lung section analysis showed that in Mtb infected mice, MSC could not be found in the proximity of the inflammatory foci. Thus, in healthy recipients, MSC administration dramatically changed T-cell function and cytokine/chemokine milieu in the lungs, most likely, due to capillary blockade. But, during Mtb infection, i.e., in the highly-inflammatory conditions, MSC did not affect T-cell function and the level of inflammation. The findings emphasize the importance of the evaluation of MSC effects locally at the site of their predominant post-injection localization and question MSC usefulness as anti-TB treatment.
[Mh] Termos MeSH primário: Pulmão/imunologia
Células Mesenquimais Estromais/fisiologia
[Mh] Termos MeSH secundário: Tecido Adiposo
Animais
Linfócitos T CD4-Positivos/metabolismo
Células Cultivadas
Quimiocina CCL2/metabolismo
Quimiocina CCL3/metabolismo
Quimiocina CCL4/metabolismo
Quimiocina CCL5/metabolismo
Quimiocina CXCL1/metabolismo
Interferon gama/metabolismo
Interleucina-10/metabolismo
Interleucina-4/metabolismo
Interleucina-5/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mycobacterium tuberculosis/imunologia
Mycobacterium tuberculosis/patogenicidade
Tuberculose Resistente a Múltiplos Medicamentos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Chemokine CCL3); 0 (Chemokine CCL4); 0 (Chemokine CCL5); 0 (Chemokine CXCL1); 0 (Interleukin-5); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178983


  7 / 1897 MEDLINE  
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[PMID]:28507028
[Au] Autor:Sprokholt JK; Kaptein TM; van Hamme JL; Overmars RJ; Gringhuis SI; Geijtenbeek TBH
[Ad] Endereço:Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, the Netherlands; and.
[Ti] Título:RIG-I-like Receptor Triggering by Dengue Virus Drives Dendritic Cell Immune Activation and T 1 Differentiation.
[So] Source:J Immunol;198(12):4764-4771, 2017 Jun 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dengue virus (DENV) causes 400 million infections annually and is one of several viruses that can cause viral hemorrhagic fever, which is characterized by uncontrolled immune activation resulting in high fever and internal bleeding. Although the underlying mechanisms are unknown, massive cytokine secretion is thought to be involved. Dendritic cells (DCs) are the main target cells of DENV, and we investigated their role in DENV-induced cytokine production and adaptive immune responses. DENV infection induced DC maturation and secretion of IL-1ß, IL-6, and TNF. Inhibition of DENV RNA replication abrogated these responses. Notably, silencing of RNA sensors RIG-I or MDA5 abrogated DC maturation, as well as cytokine responses by DENV-infected DCs. DC maturation was induced by type I IFN responses because inhibition of IFN-α/ß receptor signaling abrogated DENV-induced DC maturation. Moreover, DENV infection of DCs resulted in CCL2, CCL3, and CCL4 expression, which was abrogated after RIG-I and MDA5 silencing. DCs play an essential role in T cell differentiation, and we show that RIG-I and MDA5 triggering by DENV leads to T 1 polarization, which is characterized by high levels of IFN-γ. Notably, cytokines IL-6, TNF, and IFN-γ and chemokines CCL2, CCL3, and CCL4 have been associated with disease severity, endothelial dysfunction, and vasodilation. Therefore, we identified RIG-I and MDA5 as critical players in innate and adaptive immune responses against DENV, and targeting these receptors has the potential to decrease hemorrhagic fever in patients.
[Mh] Termos MeSH primário: Proteína DEAD-box 58/imunologia
Células Dendríticas/imunologia
Vírus da Dengue/imunologia
Células Th1/imunologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CCL3/genética
Quimiocina CCL3/imunologia
Quimiocina CCL4/genética
Quimiocina CCL4/imunologia
Proteína DEAD-box 58/deficiência
Proteína DEAD-box 58/genética
Proteína DEAD-box 58/metabolismo
Células Dendríticas/virologia
Seres Humanos
Helicase IFIH1 Induzida por Interferon/deficiência
Helicase IFIH1 Induzida por Interferon/imunologia
Helicase IFIH1 Induzida por Interferon/secreção
Interferon gama/imunologia
Interferon gama/secreção
Interleucina-1beta/imunologia
Interleucina-1beta/secreção
Interleucina-6/imunologia
Interleucina-6/secreção
Células Th1/fisiologia
Fator de Necrose Tumoral alfa/imunologia
Fator de Necrose Tumoral alfa/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (CCL3 protein, human); 0 (CCL4 protein, human); 0 (Chemokine CCL2); 0 (Chemokine CCL3); 0 (Chemokine CCL4); 0 (IL6 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma); EC 3.6.1.- (DDX58 protein, human); EC 3.6.1.- (IFIH1 protein, human); EC 3.6.4.13 (DEAD Box Protein 58); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602121


  8 / 1897 MEDLINE  
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[PMID]:28373581
[Au] Autor:Dragoni S; Hudson N; Kenny BA; Burgoyne T; McKenzie JA; Gill Y; Blaber R; Futter CE; Adamson P; Greenwood J; Turowski P
[Ad] Endereço:Department of Cell Biology, Institute of Ophthalmology, University College London, London EC1V 9EL, United Kingdom.
[Ti] Título:Endothelial MAPKs Direct ICAM-1 Signaling to Divergent Inflammatory Functions.
[So] Source:J Immunol;198(10):4074-4085, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lymphocyte transendothelial migration (TEM) is critically dependent on intraendothelial signaling triggered by adhesion to ICAM-1. Here we show that endothelial MAPKs ERK, p38, and JNK mediate diapedesis-related and diapedesis-unrelated functions of ICAM-1 in cerebral and dermal microvascular endothelial cells (MVECs). All three MAPKs were activated by ICAM-1 engagement, either through lymphocyte adhesion or Ab-mediated clustering. MAPKs were involved in ICAM-1-dependent expression of TNF-α in cerebral and dermal MVECs, and CXCL8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs. Endothelial JNK and to a much lesser degree p38 were the principal MAPKs involved in facilitating diapedesis of CD4 lymphocytes across both types of MVECs, whereas ERK was additionally required for TEM across dermal MVECs. JNK activity was critical for ICAM-1-induced F-actin rearrangements. Furthermore, activation of endothelial ICAM-1/JNK led to phosphorylation of paxillin, its association with VE-cadherin, and internalization of the latter. Importantly ICAM-1-induced phosphorylation of paxillin was required for lymphocyte TEM and converged functionally with VE-cadherin phosphorylation. Taken together we conclude that during lymphocyte TEM, ICAM-1 signaling diverges into pathways regulating lymphocyte diapedesis, and other pathways modulating gene expression thereby contributing to the long-term inflammatory response of the endothelium.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Inflamação/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Transdução de Sinais
Migração Transendotelial e Transepitelial
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Encéfalo/irrigação sanguínea
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/fisiologia
Movimento Celular
Células Cultivadas
Quimiocina CCL3/genética
Quimiocina CCL3/imunologia
Quimiocina CCL4/genética
Quimiocina CCL4/imunologia
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Derme/irrigação sanguínea
Células Endoteliais/imunologia
Endotélio Vascular/citologia
Endotélio Vascular/imunologia
Endotélio Vascular/metabolismo
Ativação Enzimática
Seres Humanos
Inflamação/imunologia
Interleucina-8/genética
Interleucina-8/imunologia
Sistema de Sinalização das MAP Quinases
Microvasos
Paxilina/metabolismo
Fosforilação
Fator de Necrose Tumoral alfa/metabolismo
Molécula 1 de Adesão de Célula Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CCL3 protein, human); 0 (CCL4 protein, human); 0 (Chemokine CCL3); 0 (Chemokine CCL4); 0 (ICAM1 protein, human); 0 (IL8 protein, human); 0 (Interleukin-8); 0 (PXN protein, human); 0 (Paxillin); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600823


  9 / 1897 MEDLINE  
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[PMID]:28341057
[Au] Autor:Kim YH; Lee JK
[Ad] Endereço:Department of Biology Education, College of Education, Chungbuk National University, Cheongju, Chungbuk 361-763, Republic of Korea.
[Ti] Título:Histone deacetylase inhibitors suppress immature dendritic cell's migration by regulating CC chemokine receptor 1 expression.
[So] Source:Cell Immunol;316:11-20, 2017 Jun.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The modulation of immature dendritic cells (iDCs), which involves processes such as phagocytosis, migration, and maturation, is considered a beneficial research theme. Once activated by an antigen, iDCs turn to mature DCs (mDCs) and migrate towards secondary lymphoid organs, and initiate the progress of cellular immunity. Histone deacetylase inhibitors (HDACis) are also thought to be a major modulator of cellular immunity. Herein, we demonstrate that HDACis (trichostatin-A (TSA), sodium butylate (SB), scriptaid (ST)) play a central regulatory role in the migratory activity of iDCs. In our results, TSA, SB and ST showed the potent inhibitory effect on the migration of iDCs stimulated by MIP-1α. The inhibitory activities of HDACis were found to be caused by reduction of CCR1 expression on the cell surface, and by the inhibition of phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases 1 and 2 (ERK 1/2), and c-Jun N-terminal kinase (JNK).
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Células Dendríticas
Inibidores de Histona Desacetilases/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácido Butírico/farmacologia
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Quimiocina CCL3/farmacologia
Células Dendríticas/citologia
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Regulação para Baixo
Ácidos Hidroxâmicos/farmacologia
Hidroxilaminas/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Quinolinas/farmacologia
Receptores CCR1/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl3 protein, mouse); 0 (Chemokine CCL3); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Hydroxylamines); 0 (Quinolines); 0 (Receptors, CCR1); 0 (scriptaid); 107-92-6 (Butyric Acid); 3X2S926L3Z (trichostatin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE


  10 / 1897 MEDLINE  
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[PMID]:28329080
[Au] Autor:Lofgren S; Hullsiek KH; Morawski BM; Nabeta HW; Kiggundu R; Taseera K; Musubire A; Schutz C; Abassi M; Bahr NC; Tugume L; Muzoora C; Williams DA; Rolfes MA; Velamakanni SS; Rajasingham R; Meintjes G; Rhein J; Meya DB; Boulware DR; COAT and ASTRO-CM Trial Teams
[Ad] Endereço:University of Minnesota, Minneapolis, MN, USA.
[Ti] Título:Differences in Immunologic Factors Among Patients Presenting with Altered Mental Status During Cryptococcal Meningitis.
[So] Source:J Infect Dis;215(5):693-697, 2017 03 01.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Altered mental status in cryptococcal meningitis results in poorer survival, but underlying causes of altered mentation are poorly understood. Within two clinical trials, we assessed risk factors for altered mental status (GCS score<15) considering baseline clinical characteristics, CSF cytokines/chemokines, and antiretroviral therapy. Among 326 enrolled participants, 97 (30%) had GCS<15 and these patients had lower median CSF cryptococcal antigen titers (P = .042) and CCL2 (P = .005) but higher opening pressures (320 vs. 269 mm H2O; P = .016), IL-10 (P = .044), and CCL3 (P = .008) compared with persons with GCS=15. Altered mental status may be associated with host immune response rather than Cryptococcus burden.
[Mh] Termos MeSH primário: Quimiocina CCL3/sangue
Interleucina-10/sangue
Meningite Criptocócica/sangue
Transtornos Mentais/sangue
[Mh] Termos MeSH secundário: Adulto
Antifúngicos/uso terapêutico
Antígenos de Fungos/sangue
Quimiocinas/sangue
Cryptococcus neoformans
Citocinas/sangue
Feminino
Seres Humanos
Masculino
Meningite Criptocócica/tratamento farmacológico
Meningite Criptocócica/imunologia
Transtornos Mentais/imunologia
Projetos Piloto
Modelos de Riscos Proporcionais
Estudos Prospectivos
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antifungal Agents); 0 (Antigens, Fungal); 0 (CCL3 protein, human); 0 (Chemokine CCL3); 0 (Chemokines); 0 (Cytokines); 0 (IL10 protein, human); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix033



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