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[PMID]:29380441
[Au] Autor:Waugh CA; Arukwe A; Jaspers VLB
[Ad] Endereço:Environmental Toxicology, Department of Biology, Faculty of Natural Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
[Ti] Título:Deregulation of microRNA-155 and its transcription factor NF-kB by polychlorinated biphenyls during viral infections.
[So] Source:APMIS;126(3):234-240, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Polychlorinated biphenyls (PCBs), and similar environmental contaminants, have been linked to virus outbreaks and increased viral induced mortality since the 1970s. Yet the mechanisms behind this increased susceptibility remain elusive. It has recently been illustrated that the innate immune viral detection system is tightly regulated by small non-coding RNAs, including microRNAs (miRNAs). For virus infections miRNA-155 expression is an important host response against infection, and deregulation of this miRNA is closely associated with adverse outcomes. Thus, we designed a targeted in vitro study using primary chicken fibroblasts, first exposed to a mixture of PCBs (Arochlor-1250) before being stimulated with a synthetic RNA virus (poly I:C), to determine if PCBs have the potential to deregulate miRNA-155. In this paper, we provide the first data for the deregulation of miRNA-155 when a host is exposed to a mixture of PCBs before a virus infection. Thus, we provide important evidence that PCBs can be involved in the deregulation of important miRNA pathways involved in the immune system; thereby demonstrating novel insights into the mechanism of PCB toxicity on the immune system.
[Mh] Termos MeSH primário: Imunidade Inata/genética
MicroRNAs/genética
NF-kappa B/genética
Poli I-C/farmacologia
Bifenilos Policlorados/química
Vírus/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Embrião de Galinha
Galinhas/genética
Galinhas/imunologia
Regulação da Expressão Gênica/imunologia
Seres Humanos
Viroses/genética
Viroses/imunologia
Viroses/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); DFC2HB4I0K (Polychlorinated Biphenyls); O84C90HH2L (Poly I-C)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12811


  2 / 4705 MEDLINE  
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[PMID]:28453927
[Au] Autor:Gentle IE; McHenry KT; Weber A; Metz A; Kretz O; Porter D; Häcker G
[Ad] Endereço:Faculty of Medicine, Institute for Medical Microbiology and Hygiene, Medical Center - University of Freiburg, University of Freiburg, Germany.
[Ti] Título:TIR-domain-containing adapter-inducing interferon-ß (TRIF) forms filamentous structures, whose pro-apoptotic signalling is terminated by autophagy.
[So] Source:FEBS J;284(13):1987-2003, 2017 07.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The formation of amyloid-like protein structures has recently emerged as a feature in signal transduction, particularly in innate immunity. These structures appear to depend on defined domains for their formation but likely also require dedicated ways to terminate signalling. We, here, define the innate immunity protein/Toll-like receptor adaptor TIR-domain-containing adapter-inducing interferon-ß (TRIF) as a novel platform of fibril formation and probe signal initiation through TRIF as well as its termination in Toll-like receptor 3 (TLR3)-stimulated melanoma cells. A main signalling pathway triggered by TLR3 caused apoptosis, which was controlled by inhibitor of apoptosis proteins and was dependent on RIPK1 and independent of TNF. Using correlative electron/fluorescence microscopy, we visualised fibrillar structures formed through both Toll/interleukin-1 receptor and RIP homotypic interacting motif regions of TRIF. We provide evidence that these fibrillary structures are active signalling platforms whose activity is terminated by autophagy. TRIF-signalling enhanced autophagy, and fibrillary structures were partly contained within autophagosomes. Inhibition of autophagy increased levels of pro-apoptotic TRIF complexes, leading to the accumulation of active caspase-8 and enhanced apoptosis while stimulation of autophagy reduced TRIF-dependent death. We conclude that pro-death signals through TRIF are regulated by autophagy and propose that pro-apoptotic signalling through TRIF/RIPK1/caspase-8 occurs in fibrillary platforms.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Apoptose/fisiologia
Autofagia/fisiologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/química
Proteínas Adaptadoras de Transporte Vesicular/genética
Animais
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Western Blotting
Caspase 8/genética
Caspase 8/metabolismo
Linhagem Celular Tumoral
Células Cultivadas
Células HEK293
Células HeLa
Seres Humanos
Camundongos Knockout
Microscopia Eletrônica de Transmissão
Microscopia de Fluorescência
Oligopeptídeos/farmacologia
Poli I-C/farmacologia
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Receptor 3 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (LBW242); 0 (Oligopeptides); 0 (TICAM1 protein, human); 0 (Toll-Like Receptor 3); EC 2.7.11.1 (RIPK1 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 3.4.22.- (Caspase 8); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14091


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[PMID]:27771388
[Au] Autor:Martinez EC; Garg R; Shrivastava P; Gomis S; van Drunen Littel-van den Hurk S
[Ad] Endereço:Department of Microbiology and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, 107 Wiggins Road, S7N 5E5, Canada; Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-InterVac), University of Saskatchewan, Saskatoon, Saskatchewan, 120 V
[Ti] Título:Intranasal treatment with a novel immunomodulator mediates innate immune protection against lethal pneumonia virus of mice.
[So] Source:Antiviral Res;135:108-119, 2016 11.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Respiratory syncytial virus (RSV) is the leading cause of acute lower respiratory tract infections in infants and young children. There are no licensed RSV vaccines available, and the few treatment options for high-risk individuals are either extremely costly or cause severe side effects and toxicity. Immunomodulation mediated by a novel formulation consisting of the toll-like receptor 3 agonist poly(I:C), an innate defense regulator peptide and a polyphosphazene (P-I-P) was evaluated in the context of lethal infection with pneumonia virus of mice (PVM). Intranasal delivery of a single dose of P-I-P protected adult mice against PVM when given 24 h prior to challenge. These animals experienced minimal weight loss, no clinical disease, 100% survival, and reduced lung pathology. Similar clinical outcomes were observed in mice treated up to 3 days prior to infection. P-I-P pre-treatment induced early mRNA and protein expression of key chemokine and cytokine genes, reduced the recruitment of neutrophils and eosinophils, decreased virus titers in the lungs, and modulated the delayed exacerbated nature of PVM disease without any short-term side effects. On day 14 post-infection, P-I-P-treated mice were confirmed to be PVM-free. These results demonstrate the capacity of this formulation to prevent PVM and possibly other viral respiratory infections.
[Mh] Termos MeSH primário: Imunidade Inata
Fatores Imunológicos/administração & dosagem
Vírus da Pneumonia Murina/imunologia
Compostos Organofosforados/administração & dosagem
Infecções por Pneumovirus/prevenção & controle
Poli I-C/administração & dosagem
Polímeros/administração & dosagem
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos
Administração Intranasal
Animais
Citocinas/imunologia
Fatores Imunológicos/química
Fatores Imunológicos/imunologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos BALB C
Compostos Organofosforados/imunologia
Infecções por Pneumovirus/imunologia
Poli I-C/imunologia
Receptor 3 Toll-Like/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Cytokines); 0 (Immunologic Factors); 0 (Organophosphorus Compounds); 0 (Polymers); 0 (Toll-Like Receptor 3); 0 (poly(phosphazene)); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


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[PMID]:28747347
[Au] Autor:Ye W; Hu MM; Lei CQ; Zhou Q; Lin H; Sun MS; Shu HB
[Ad] Endereço:College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, China; and.
[Ti] Título:TRIM8 Negatively Regulates TLR3/4-Mediated Innate Immune Response by Blocking TRIF-TBK1 Interaction.
[So] Source:J Immunol;199(5):1856-1864, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TLR-mediated signaling pathways play critical roles in host defense against microbials. However, dysregulation of innate immune and inflammatory responses triggered by TLRs would result in harmful damage to the host. Using a gene-knockout mouse model, we show that tripartite motif (TRIM) 8 negatively regulates TLR3- and TLR4-mediated innate immune and inflammatory responses. TRIM8 deficiency leads to increased polyinosinic-polycytidylic acid- and LPS-triggered induction of downstream anti-microbial genes including , , , and , evaluated serum cytokine levels, and increased susceptibility of mice to polyinosinic-polycytidylic acid- and LPS-induced inflammatory death as well as infection-induced loss of body weight and septic shock. TRIM8 interacted with Toll/IL-1 receptor domain-containing adapter-inducing IFN-ß and mediated its K6- and K33-linked polyubiquitination, leading to disruption of the Toll/IL-1 receptor domain-containing adapter-inducing IFN-ß-TANK-binding kinase-1 association. Our findings uncover an additional mechanism on the termination of TLR3/4-mediated inflammatory and innate immune responses.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Proteínas de Transporte/metabolismo
Inflamação/imunologia
Proteínas do Tecido Nervoso/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Infecções por Salmonella/imunologia
Salmonella typhimurium/imunologia
Choque Séptico/imunologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte/genética
Citocinas/genética
Citocinas/metabolismo
Células HEK293
Seres Humanos
Imunidade Inata
Inflamação/microbiologia
Mediadores da Inflamação/metabolismo
Lipopolissacarídeos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas do Tecido Nervoso/genética
Poli I-C/imunologia
Ligação Proteica
Transdução de Sinais
Receptor 3 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Carrier Proteins); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Lipopolysaccharides); 0 (Nerve Tissue Proteins); 0 (TICAM-1 protein, mouse); 0 (TLR3 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 3); 0 (Toll-Like Receptor 4); 0 (Trim8 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (TBK1 protein, human); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601647


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[PMID]:29253904
[Au] Autor:Silver AC
[Ad] Endereço:Department of Biology, University of Hartford, West Hartford, CT, United States.
[Ti] Título:Pathogen-associated molecular patterns alter molecular clock gene expression in mouse splenocytes.
[So] Source:PLoS One;12(12):e0189949, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Circadian rhythms are endogenous 24-h oscillations that influence a multitude of physiological processes. The pathogen-associated molecular pattern (PAMP), lipopolysaccharide, has been shown to modify the circadian molecular clock. The aim of this study was to determine if other PAMPs alter clock gene expression. Therefore, mRNA levels of clock genes (Per2, Bmal1, Rev-erbα, and Dbp) were measured after an ex vivo challenge with several PAMPs and to further test the relevance of PAMP alteration of the molecular clock, an in vivo poly(I:C) challenge was performed. This study revealed that several other PAMPs are also capable of altering clock gene expression.
[Mh] Termos MeSH primário: Proteínas CLOCK/metabolismo
Relógios Circadianos/genética
Padrões Moleculares Associados a Patógenos/metabolismo
Baço/citologia
[Mh] Termos MeSH secundário: Fatores de Transcrição ARNTL/genética
Animais
Proteínas CLOCK/genética
Ritmo Circadiano
Expressão Gênica
Regulação da Expressão Gênica
Ligantes
Lipopolissacarídeos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C/imunologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (Ligands); 0 (Lipopolysaccharides); 0 (Pathogen-Associated Molecular Pattern Molecules); 0 (RNA, Messenger); EC 2.3.1.48 (CLOCK Proteins); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189949


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[PMID]:27773730
[Au] Autor:Wang TY; Chen YM; Chen TY
[Ad] Endereço:Laboratory of Molecular Genetics, Institute of Biotechnology, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 70101, Taiwan; Translational Center for Marine Biotechnology, National Cheng Kung University, Tainan 70101, Taiwan.
[Ti] Título:Molecular cloning of orange-spotted grouper (Epinephelus coioides) heat shock transcription factor 1 isoforms and characterization of their expressions in response to nodavirus.
[So] Source:Fish Shellfish Immunol;59:123-136, 2016 Dec.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Heat shock transcription factor 1 (HSF1) regulates heat shock proteins (HSPs), which assist in protein folding and inhibit protein denaturation following stress. HSF1 was firstly cloned from orange-spotted grouper and exists as two isoforms, one with (osgHSF1a) and one without (osgHSF1b) exon 11. Heat exposure increased the expression of osgHSF1b while cold exposure increased that of osgHSF1a. Both isoforms were mainly expressed in the brains, eyes, and fins. Expression of osgHSF1b was higher than osgHSF1a during development. Poly I:C and LPS could also induce osgHSF1 isoforms expression differentially. Exposure to nervous necrosis virus (NNV) increased the level of both osgHSF1 isoforms at 12 h. GF-1 cells with overexpression of osgHSF1 isoforms enhanced viral loads within 24 h, whereas both pharmacological inhibition and RNA interference of HSF1 reduced virus infection. This study shows that osgHSF1 can support the early stage of virus infection and provides a new insight into the molecular regulation of osgHSF1 between the influence of temperatures and immunity.
[Mh] Termos MeSH primário: Bass
Proteínas de Ligação a DNA/genética
Doenças dos Peixes/imunologia
Proteínas de Peixes/genética
Regulação da Expressão Gênica/imunologia
Infecções por Vírus de RNA/veterinária
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Clonagem Molecular
DNA Complementar/genética
DNA Complementar/metabolismo
Proteínas de Ligação a DNA/química
Proteínas de Ligação a DNA/metabolismo
Proteínas de Peixes/química
Proteínas de Peixes/metabolismo
Fatores de Transcrição de Choque Térmico
Temperatura Alta/efeitos adversos
Imunidade/efeitos dos fármacos
Lipopolissacarídeos/farmacologia
Nodaviridae/fisiologia
Filogenia
Poli I-C/farmacologia
Isoformas de Proteínas/química
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Infecções por Vírus de RNA/imunologia
Alinhamento de Sequência/veterinária
Fatores de Transcrição/química
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (DNA-Binding Proteins); 0 (Fish Proteins); 0 (Heat Shock Transcription Factors); 0 (Lipopolysaccharides); 0 (Protein Isoforms); 0 (Transcription Factors); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171203
[Lr] Data última revisão:
171203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:28910320
[Au] Autor:Muire PJ; Hanson LA; Wills R; Petrie-Hanson L
[Ad] Endereço:Department of Basic Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, Mississippi, United States of America.
[Ti] Título:Differential gene expression following TLR stimulation in rag1-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations.
[So] Source:PLoS One;12(9):e0184077, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the absence of lymphocytes, rag1-/- mutant zebrafish develop protective immunity to bacteria. In mammals, induction of protection by innate immunity can be mediated by macrophages or natural killer (NK) cells. To elucidate potential responsive cell populations, we morphologically characterized lymphocyte-like cells (LLCs) from liver, spleen and kidney hematopoietic tissues. In fish, these cells include NK cells and Non-specific cytotoxic cells (NCCs). We also evaluated the transcriptional expression response of select genes that are important indicators of NK and macrophage activation after exposure to specific TLR ligands. The LLC cell populations could be discriminated by size and further discriminated by the presence of cytoplasmic granules. Expression levels of mx, tnfα, ifnγ, t-bet and nitr9 demonstrated dynamic changes in response to intra-coelomically administered ß glucan (a TLR2/6 ligand), Poly I:C (a TLR3 ligand) and resiquimod (R848) (a TLR7/8 ligand). Following TLR 2/6 stimulation, there was a greater than 100 fold increase in ifnγ in liver, kidney and spleen and moderate increases in tnfα in liver and kidney. TLR3 stimulation caused broad up regulation of mx, down-regulation of tnfα in kidney and spleen tissues and up regulation of nitr9 in the kidney. Following TLR 7/8 stimulation, there was a greater than 100 fold increase in ifnγ in liver and kidney and t-bet in liver. Our gene expression findings suggest that LLCs and macrophages are stimulated following ß glucan exposure. Poly I:C causes type I interferon response and mild induction of LLC in the kidney and R-848 exposure causes the strongest LLC stimulation. Overall, the strongest NK like gene expression occurred in the liver. These differential effects of TLR ligands in rag1-/- mutant zebrafish shows strong NK cell-like gene expression responses, especially in the liver, and provides tools to evaluate the basis for protective immunity mediated by the innate immune cells of fish.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/imunologia
Proteínas de Homeodomínio/imunologia
Linfócitos/imunologia
Receptores Toll-Like/imunologia
Proteínas de Peixe-Zebra/imunologia
Peixe-Zebra/imunologia
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Proteínas de Homeodomínio/genética
Imidazóis/farmacologia
Imunidade Inata/efeitos dos fármacos
Imunidade Inata/genética
Macrófagos/imunologia
Especificidade de Órgãos/efeitos dos fármacos
Especificidade de Órgãos/genética
Especificidade de Órgãos/imunologia
Poli I-C/farmacologia
Receptores Toll-Like/agonistas
Peixe-Zebra/genética
Proteínas de Peixe-Zebra/genética
beta-Glucanas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Imidazoles); 0 (Toll-Like Receptors); 0 (Zebrafish Proteins); 0 (beta-Glucans); 128559-51-3 (RAG-1 protein); O84C90HH2L (Poly I-C); V3DMU7PVXF (resiquimod)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184077


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[PMID]:28882453
[Au] Autor:Tharuka MDN; Bathige SDNK; Lee J
[Ad] Endereço:Department of Marine Life Sciences & Fish Vaccine Research Center, Jeju National University, Jeju Self-Governing Province 63243, Republic of Korea.
[Ti] Título:Molecular cloning, biochemical characterization, and expression analysis of two glutathione S-transferase paralogs from the big-belly seahorse (Hippocampus abdominalis).
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;214:1-11, 2017 Dec.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glutathione S-transferases (GSTs, EC 2.5.1.18) are important Phase II detoxifying enzymes that catalyze hydrophobic, electrophilic xenobiotic substance with the conjugation of reduced glutathione (GSH). In this study, GSTµ and GSTρ paralogs of GST in the big belly seahorse (Hippocampus abdominalis; HaGSTρ, HaGSTµ) were biochemically, molecularly, functionally characterized to determine their detoxification range and protective capacities upon different pathogenic stresses. HaGSTρ and HaGSTµ are composed of coding sequences of 681bp and 654bp, which encode proteins 225 and 217 amino acids, with predicted molecular masses of 26.06kDa and 25.74kDa respectively. Sequence analysis revealed that both HaGSTs comprise the characteristic GSH-binding site in the thioredoxin-like N-terminal domain and substrate binding site in the C-terminal domain. The recombinant HaGSTρ and HaGSTµ proteins catalyzed the model GST substrate 1-chloro-2, 4-dinitrobenzene (CDNB). Enzyme kinetic analysis revealed different K and V values for each rHaGST, suggesting that they have different conjugation rates. The optimum conditions (pH, temperature) and inhibitory assays of each protein demonstrated different optimal ranges. However, HaGSTµ was highly expressed in the ovary and gill, whereas HaGSTρ was highly expressed in the gill and pouch. mRNA expression of HaGSTρ and HaGSTµ was significantly elevated upon lipopolysaccharide, Poly (I:C), and Edwardsiella tarda challenges in liver and in blood cells as well as with Streptococcus iniae challenge in blood cells. From these collective experimental results, we propose that HaGSTρ and HaGSTµ are effective in detoxifying xenobiotic toxic agents, and importantly, their mRNA expression could be stimulated by immunological stress signals in the aquatic environment.
[Mh] Termos MeSH primário: Proteínas de Peixes/química
Glutationa Transferase/química
Smegmamorpha/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação
Clonagem Molecular
Dinitroclorobenzeno/imunologia
Dinitroclorobenzeno/metabolismo
Escherichia coli/genética
Escherichia coli/metabolismo
Proteínas de Peixes/agonistas
Proteínas de Peixes/genética
Proteínas de Peixes/imunologia
Expressão Gênica
Glutationa Transferase/genética
Glutationa Transferase/imunologia
Isoenzimas/química
Isoenzimas/genética
Isoenzimas/imunologia
Cinética
Lipopolissacarídeos/farmacologia
Modelos Moleculares
Especificidade de Órgãos
Filogenia
Poli I-C/farmacologia
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Estrutura Terciária de Proteína
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/imunologia
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Smegmamorpha/classificação
Smegmamorpha/imunologia
Smegmamorpha/microbiologia
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fish Proteins); 0 (Isoenzymes); 0 (Lipopolysaccharides); 0 (Recombinant Proteins); EC 2.5.1.18 (Glutathione Transferase); GE3IBT7BMN (Dinitrochlorobenzene); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  9 / 4705 MEDLINE  
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[PMID]:28835457
[Au] Autor:Roewe J; Higer M; Riehl DR; Gericke A; Radsak MP; Bosmann M
[Ad] Endereço:Center for Thrombosis and Hemostasis, University Medical Center, Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
[Ti] Título:Neuroendocrine Modulation of IL-27 in Macrophages.
[So] Source:J Immunol;199(7):2503-2514, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heterodimeric IL-27 (p28/EBV-induced gene 3) is an important member of the IL-6/IL-12 cytokine family. IL-27 is predominantly synthesized by mononuclear phagocytes and exerts immunoregulatory functional activities on lymphocytic and nonlymphocytic cells during infection, autoimmunity or neoplasms. There is a great body of evidence on the bidirectional interplay between the autonomic nervous system and immune responses during inflammatory disorders, but so far IL-27 has not been defined as a part of these multifaceted neuroendocrine networks. In this study, we describe the role of catecholamines (as mediators of the sympathetic nervous system) related to IL-27 production in primary mouse macrophages. Noradrenaline and adrenaline dose-dependently suppressed the release of IL-27p28 in LPS/TLR4-activated macrophages, which was independent of α adrenoceptors. Instead, ß adrenoceptor activation was responsible for mediating gene silencing of IL-27p28 and EBV-induced gene 3. The ß adrenoceptor agonists formoterol and salbutamol mediated suppression of IL-27p28 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spared the polyinosinic-polycytidylic acid/TLR3 pathway. Mechanistically, ß adrenergic signaling reinforced an autocrine feedback loop of macrophage-derived IL-10 and this synergized with inhibition of the JNK pathway for limiting IL-27p28. The JNK inhibitors SP600125 and AEG3482 strongly decreased intracellular IL-27p28 in F4/80 CD11b macrophages. In endotoxic shock of C57BL/6J mice, pharmacologic activation of ß adrenoceptors improved the severity of shock, including hypothermia and decreased circulating IL-27p28. Conversely, IL-27p28 was 2.7-fold increased by removal of the catecholamine-producing adrenal glands prior to endotoxic shock. These data suggest a novel role of the sympathetic neuroendocrine system for the modulation of IL-27-dependent acute inflammation.
[Mh] Termos MeSH primário: Epinefrina/farmacologia
Interleucinas/imunologia
Interleucinas/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Norepinefrina/farmacologia
[Mh] Termos MeSH secundário: Albuterol/farmacologia
Animais
Antracenos/farmacologia
Células Cultivadas
Fumarato de Formoterol/farmacologia
Inflamação
Interleucina-10/biossíntese
Interleucina-10/imunologia
Interleucinas/sangue
Interleucinas/genética
Lipopolissacarídeos/farmacologia
Ativação de Macrófagos/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C/metabolismo
Receptores Adrenérgicos/efeitos dos fármacos
Choque Séptico
Transdução de Sinais/efeitos dos fármacos
Sulfonamidas/farmacologia
Sistema Nervoso Simpático/imunologia
Sistema Nervoso Simpático/fisiologia
Tiadiazóis/farmacologia
Receptor 3 Toll-Like/metabolismo
Zimosan/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AEG 3482); 0 (Anthracenes); 0 (Il27 protein, mouse); 0 (Interleukins); 0 (Lipopolysaccharides); 0 (Receptors, Adrenergic); 0 (Sulfonamides); 0 (Thiadiazoles); 0 (Toll-Like Receptor 3); 130068-27-8 (Interleukin-10); 1TW30Y2766 (pyrazolanthrone); 9010-72-4 (Zymosan); O84C90HH2L (Poly I-C); QF8SVZ843E (Albuterol); W34SHF8J2K (Formoterol Fumarate); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700687


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[PMID]:28778432
[Au] Autor:McCabe K; Concannon RM; McKernan DP; Dowd E
[Ad] Endereço:Pharmacology & Therapeutics, National University of Ireland, Galway, Ireland; Galway Neuroscience Centre, National University of Ireland, Galway, Ireland.
[Ti] Título:Time-course of striatal Toll-like receptor expression in neurotoxic, environmental and inflammatory rat models of Parkinson's disease.
[So] Source:J Neuroimmunol;310:103-106, 2017 Sep 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Because Toll-like receptors (TLRs) are emerging as potential targets for anti-inflammatory intervention in neurodegenerative diseases, the aim of this study was to characterise the time-course of TLR expression in neurotoxic, environmental and inflammatory Parkinson's disease models. Male Sprague Dawley rats were given intra-striatal injections of 6-hydroxydopamine (10µg), rotenone (1.25µg), LPS (10µg) or Poly I:C (20µg) and were sacrificed on Days 1, 4, 14 and 28 post surgery. Changes in the expression of several inflammatory markers, including TLR3, TLR4 and selected cytokines, were examined using qRT-PCR. We found pronounced changes in the bacterial responsive TLR4 and the viral responsive TLR3 receptors in the inflamed striatum in all models, regardless of whether the challenge was neurotoxic, environmental or inflammatory in nature. However, the magnitude and time-course of changes in expression was different between the different models. This study highlights the pattern of changes in TLR expression in models of Parkinson's disease, and further strengthens the rationale for targeting TLRs for anti-inflammatory intervention in this neurodegenerative disease.
[Mh] Termos MeSH primário: Corpo Estriado/metabolismo
Oxidopamina/toxicidade
Doença de Parkinson
Poli I-C/toxicidade
Rotenona/toxicidade
Receptores Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Corpo Estriado/efeitos dos fármacos
Citocinas/metabolismo
Modelos Animais de Doenças
Regulação da Expressão Gênica/efeitos dos fármacos
Doença de Parkinson/etiologia
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
Ratos
Ratos Sprague-Dawley
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Toll-Like Receptors); 03L9OT429T (Rotenone); 8HW4YBZ748 (Oxidopamine); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE



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