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Pesquisa : D12.644.360.024.311 [Categoria DeCS]
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[PMID]:28471051
[Au] Autor:Döring C; Regen T; Gertig U; van Rossum D; Winkler A; Saiepour N; Brück W; Hanisch UK; Janova H
[Ad] Endereço:Institute of Neuropathology, University Medical Center Göttingen, Göttingen, 37075, Germany.
[Ti] Título:A presumed antagonistic LPS identifies distinct functional organization of TLR4 in mouse microglia.
[So] Source:Glia;65(7):1176-1185, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglia as principle innate immune cells of the central nervous system (CNS) are the first line of defense against invading pathogens. They are capable of sensing infections through diverse receptors, such as Toll-like receptor 4 (TLR4). This receptor is best known for its ability to recognize bacterial lipopolysaccharide (LPS), a causative agent of gram-negative sepsis and septic shock. A putative, naturally occurring antagonist of TLR4 derives from the photosynthetic bacterium Rhodobacter sphaeroides. However, the antagonistic potential of R. sphaeroides LPS (Rs-LPS) is no universal feature, since several studies suggested agonistic rather than antagonistic actions of this molecule depending on the investigated mammalian species. Here we show the agonistic versus antagonistic potential of Rs-LPS in primary mouse microglia. We demonstrate that Rs-LPS efficiently induces the release of cytokines and chemokines, which depends on TLR4, MyD88, and TRIF, but not CD14. Furthermore, Rs-LPS is able to regulate the phagocytic capacity of microglia as agonist, while it antagonizes Re-LPS-induced MHC I expression. Finally, to our knowledge, we are the first to provide in vivo evidence for an agonistic potential of Rs-LPS, as it efficiently triggers the recruitment of peripheral immune cells to the endotoxin-challenged CNS. Together, our results argue for a versatile and complex organization of the microglial TLR4 system, which specifically translates exogenous signals into cellular functions. Importantly, as demonstrated here for microglia, the antagonistic potential of Rs-LPS needs to be considered with caution, as reactions to Rs-LPS not only differ by cell type, but even by function within one cell type.
[Mh] Termos MeSH primário: Lipopolissacarídeos/farmacologia
Microglia/efeitos dos fármacos
Receptor 4 Toll-Like/antagonistas & inibidores
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/genética
Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Animais
Animais Recém-Nascidos
Encéfalo/citologia
Células Cultivadas
Corpo Estriado/efeitos dos fármacos
Citocinas/metabolismo
Relação Dose-Resposta a Droga
Receptores de Lipopolissacarídeos/genética
Receptores de Lipopolissacarídeos/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Bainha de Mielina/efeitos dos fármacos
Bainha de Mielina/patologia
Fator 88 de Diferenciação Mieloide/genética
Fator 88 de Diferenciação Mieloide/metabolismo
Fagocitose/efeitos dos fármacos
Fagocitose/fisiologia
Receptor 4 Toll-Like/genética
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Cytokines); 0 (Lipopolysaccharide Receptors); 0 (Lipopolysaccharides); 0 (Myeloid Differentiation Factor 88); 0 (TICAM-1 protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23151


  2 / 3753 MEDLINE  
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[PMID]:29181840
[Au] Autor:Treon SP; Gustine J; Xu L; Manning RJ; Tsakmaklis N; Demos M; Meid K; Guerrera ML; Munshi M; Chan G; Chen J; Kofides A; Patterson CJ; Yang G; Liu X; Severns P; Dubeau T; Hunter ZR; Castillo JJ
[Ad] Endereço:Bing Center for Waldenstrom's Macroglobulinemia, Dana Farber Cancer Institute, Boston, MA, USA.
[Ti] Título:MYD88 wild-type Waldenstrom Macroglobulinaemia: differential diagnosis, risk of histological transformation, and overall survival.
[So] Source:Br J Haematol;180(3):374-380, 2018 02.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:MYD88 mutations are present in 95% of Waldenstrom Macroglobulinaemia (WM) patients, and support diagnostic discrimination from other IgM-secreting B-cell malignancies. Diagnostic discrimination can be difficult among suspected wild-type MYD88 (MYD88 ) WM cases. We systematically reviewed the clinical, pathological and laboratory studies for 64 suspected MYD88 WM patients. World Health Organization and WM consensus guidelines were used to establish clinicopathological diagnosis. Up to 30% of suspected MYD88 WM cases had an alternative clinicopathological diagnosis, including IgM multiple myeloma. The estimated 10-year survival was 73% (95% confidence interval [CI] 52-86%) for MYD88 versus 90% (95% CI 82-95%) for mutated (MYD88 ) WM patients (Log-rank P < 0·001). Multivariate analysis only showed MYD88 mutation status (P < 0·001) as a significant determinant for overall survival. Diffuse large B-cell lymphoma (DLBCL) was diagnosed in 7 (15·2%) and 2 (0·76%) of MYD88 and MYD88 patients, respectively (Odds ratio 23·3; 95% CI 4·2-233·8; P < 0·001). Overall survival was shorter among MYD88 patients with an associated DLBCL event (Log-rank P = 0·08). The findings show that among suspected MYD88 WM cases, an alternative clinicopathological diagnosis is common and can impact clinical care. WM patients with MYD88 disease have a high incidence of associated DLBCL events and significantly shorter survival versus those with MYD88 disease.
[Mh] Termos MeSH primário: Fator 88 de Diferenciação Mieloide/genética
Macroglobulinemia de Waldenstrom/diagnóstico
Macroglobulinemia de Waldenstrom/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores
Medula Óssea/patologia
Transformação Celular Neoplásica
Análise Mutacional de DNA
Diagnóstico Diferencial
Feminino
Genótipo
Seres Humanos
Imunofenotipagem
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Mutação
Prognóstico
Modelos de Riscos Proporcionais
Macroglobulinemia de Waldenstrom/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (MYD88 protein, human); 0 (Myeloid Differentiation Factor 88)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.15049


  3 / 3753 MEDLINE  
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[PMID]:27776995
[Au] Autor:Rebl A; Rebl H; Köbis JM; Goldammer T; Seyfert HM
[Ad] Endereço:Leibniz Institute for Farm Animal Biology (FBN), Institute for Genome Biology, Wilhelm-Stahl-Allee 2, 18196, Dummerstorf, Germany.
[Ti] Título:ST2 from rainbow trout quenches TLR signalling, localises at the nuclear membrane and allows the nuclear translocation of MYD88.
[So] Source:Dev Comp Immunol;67:139-152, 2017 02.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mammalian interleukin 1 receptor-like 1 receptor (IL1RL1), commonly known as ST2, is thought to downregulate TLR signalling by sequestering the signalling adapter MYD88 (myeloid differentiation primary response protein 88). ST2 sequences are known in several fish species, but none of them have functionally been examined. We characterised ST2 from rainbow trout (Oncorhynchus mykiss) and the structure of its encoding gene. The primary sequence of ST2 is only weakly conserved from fish to human. However, the amino acid sequences forming the interfaces for ST2 and MYD88 interaction are well conserved throughout evolution. High similarity of the gene segmentation unambiguously proves the common ancestry of fish and mammalian ST2. Trout ST2 and trout MYD88 genes were constitutively expressed in embryonic, larval and adult trout. In vivo infection with Aeromonas salmonicida did not modulate the mRNA levels of both factors. Overexpressing trout ST2 in the mammalian HEK-293 reconstitution system of TLR2 signalling quenched the Escherichia coli-induced activation of NF-κB and SAA promoters in a dose-dependent fashion. The expression of GFP-tagged trout ST2 in human HEK-293 or trout CHSE-214 cells surprisingly revealed that (i) ST2 localised abundantly at the nuclear membrane rather than at the cell membrane and (ii) the coexpression of both ST2 and MYD88 allowed the translocation of trout MYD88 from cytoplasm to nucleus, as assessed using confocal microscopy and Western blotting. Hence, we validated that trout ST2 is a dampener of TLR signalling and interacts with MYD88. The spatial distribution of these factors raises questions about how this repressive mechanism functions.
[Mh] Termos MeSH primário: Proteínas de Peixes/metabolismo
Proteína 1 Semelhante a Receptor de Interleucina-1/metabolismo
Fator 88 de Diferenciação Mieloide/metabolismo
Membrana Nuclear/metabolismo
Oncorhynchus mykiss/imunologia
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Evolução Biológica
Proteínas de Peixes/genética
Seres Humanos
Proteína 1 Semelhante a Receptor de Interleucina-1/genética
Mamíferos
Ligação Proteica
Transporte Proteico
Transdução de Sinais
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fish Proteins); 0 (IL1RL1 protein, human); 0 (Interleukin-1 Receptor-Like 1 Protein); 0 (Myeloid Differentiation Factor 88); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  4 / 3753 MEDLINE  
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[PMID]:29287085
[Au] Autor:Liu L; Steinle JJ
[Ad] Endereço:Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States of America.
[Ti] Título:Loss of TLR4 in mouse Müller cells inhibits both MyD88-dependent and -independent signaling.
[So] Source:PLoS One;12(12):e0190253, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Müller cells are key to metabolic and ionic regulation in the retina. They also produce a number of inflammatory mediators and are significantly affected in diabetic retinopathy. To investigate the role of toll-like receptor 4 (TLR4) in retinal Müller cells, we crossed TLR4 floxed with PDGFRα-Cre mice to eliminate TLR4 in retinal Müller cells. We performed Western blotting and ELISA analyses to determine whether loss of TLR4 affected myeloid differentiation primary response protein (MyD88)-dependent or -independent signaling, leading to reduced levels of tumor necrosis factor alpha (TNFα) and interleukin 1 beta (IL1ß) in whole retinal lysates from the TLR4 floxed and TLR4-PDGFRα-Cre mice. Data show that TLR4-PDGFRα-Cre mice have reduced levels of both the MyD88-dependent and -independent signaling pathways. These studies confirm successful development of a Müller cell-specific TLR4 knockout mouse colony. These mice have reduced MyD88-dependent and -independent signaling pathway proteins, as well as reduced TNFα and IL1ß levels. These mice can be used to dissect TLR4 signaling in disorders affecting retinal Müller cells.
[Mh] Termos MeSH primário: Células Ependimogliais/metabolismo
Fator 88 de Diferenciação Mieloide/metabolismo
Transdução de Sinais
Receptor 4 Toll-Like/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Ensaio de Imunoadsorção Enzimática
Interleucina-1beta/metabolismo
Camundongos
Camundongos Transgênicos
Receptor 4 Toll-Like/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190253


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[PMID]:28459433
[Au] Autor:Ulas T; Pirr S; Fehlhaber B; Bickes MS; Loof TG; Vogl T; Mellinger L; Heinemann AS; Burgmann J; Schöning J; Schreek S; Pfeifer S; Reuner F; Völlger L; Stanulla M; von Köckritz-Blickwede M; Glander S; Barczyk-Kahlert K; von Kaisenberg CS; Friesenhagen J; Fischer-Riepe L; Zenker S; Schultze JL; Roth J; Viemann D
[Ad] Endereço:Genomics and Immunoregulation, LIMES-Institut, University of Bonn, Bonn, Germany.
[Ti] Título:S100-alarmin-induced innate immune programming protects newborn infants from sepsis.
[So] Source:Nat Immunol;18(6):622-632, 2017 Jun.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The high risk of neonatal death from sepsis is thought to result from impaired responses by innate immune cells; however, the clinical observation of hyperinflammatory courses of neonatal sepsis contradicts this concept. Using transcriptomic, epigenetic and immunological approaches, we demonstrated that high amounts of the perinatal alarmins S100A8 and S100A9 specifically altered MyD88-dependent proinflammatory gene programs. S100 programming prevented hyperinflammatory responses without impairing pathogen defense. TRIF-adaptor-dependent regulatory genes remained unaffected by perinatal S100 programming and responded strongly to lipopolysaccharide, but were barely expressed. Steady-state expression of TRIF-dependent genes increased only gradually during the first year of life in human neonates, shifting immune regulation toward the adult phenotype. Disruption of this critical sequence of transient alarmin programming and subsequent reprogramming of regulatory pathways increased the risk of hyperinflammation and sepsis. Collectively these data suggest that neonates are characterized by a selective, transient microbial unresponsiveness that prevents harmful hyperinflammation in the delicate neonate while allowing for sufficient immunological protection.
[Mh] Termos MeSH primário: Calgranulina A/imunologia
Calgranulina B/imunologia
Imunidade Inata/imunologia
Monócitos/imunologia
Sepse Neonatal/imunologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/genética
Proteínas Adaptadoras de Transporte Vesicular/imunologia
Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Animais
Animais Recém-Nascidos
Calgranulina A/efeitos dos fármacos
Calgranulina B/efeitos dos fármacos
Epigênese Genética
Sangue Fetal
Citometria de Fluxo
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Seres Humanos
Imunidade Inata/efeitos dos fármacos
Immunoblotting
Recém-Nascido
Inflamação
Lipopolissacarídeos/farmacologia
Camundongos
Camundongos Knockout
Monócitos/efeitos dos fármacos
Fator 88 de Diferenciação Mieloide/genética
Fator 88 de Diferenciação Mieloide/imunologia
Sepse Neonatal/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptor 4 Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Calgranulin A); 0 (Calgranulin B); 0 (Lipopolysaccharides); 0 (Myeloid Differentiation Factor 88); 0 (TICAM-1 protein, mouse); 0 (TICAM1 protein, human); 0 (Toll-Like Receptor 4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3745


  6 / 3753 MEDLINE  
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[PMID]:29175418
[Au] Autor:Mitchell J; Kim SJ; Seelmann A; Veit B; Shepard B; Im E; Rhee SH
[Ad] Endereço:Department of Biological Sciences, Oakland University, Rochester, MI 48309, USA.
[Ti] Título:Src family kinase tyrosine phosphorylates Toll-like receptor 4 to dissociate MyD88 and Mal/Tirap, suppressing LPS-induced inflammatory responses.
[So] Source:Biochem Pharmacol;147:119-127, 2018 01.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Src family kinases (SFKs) are a family of protein tyrosine kinases containing nine members: Src, Lyn, Fgr, Hck, Lck, Fyn, Blk, Yes, and Ylk. Although SFK activation is a major immediate signaling event in LPS/Toll-like receptor 4 (TLR4) signaling, its precise role has remained elusive due to various contradictory results obtained from a certain SFK member-deficient mice or cells. The observed inconsistencies may be due to the compensation or redundancy by other SFKs upon a SFK deficiency. The chemical rescuing approach was suggested to induce temporal and precise SFK activation in living cells, thereby limiting the chance of cellular adaption to a SFK-deficient condition. Using the rescuing approach, we demonstrate that restoring SFK activity not only induces tyrosine phosphorylation of TLR4, but also inhibits LPS-induced NFκB and JNK1/2 activation and consequently suppresses LPS-induced cytokine production. TLR4 normally recruits TIR domain-containing adaptors in response to LPS, however, temporally restored SFK activation disrupts the LPS-induced association of MyD88 and Mal/Tirap with TLR4. Additionally, using kinase-dead SFK-Lyn (Y397/508F) and constitutively active SFK-Lyn (Y508F), we found that the kinase-dead SFK inhibits TLR4 tyrosine phosphorylation with reduced binding affinity to TLR4, while the kinase-active SFK strongly binds to TLR4 and promotes TLR4 tyrosine phosphorylation, suggesting that SFK kinase activity is required for TLR4 tyrosine phosphorylation and TLR4-SFK interaction. Together, our results demonstrate that SFK activation induces TLR4 tyrosine phosphorylation, consequently dissociating MyD88 and Mal/Tirap from TLR4 and inhibiting LPS-induced inflammatory responses, suggesting a negative feedback loop regulated by SFK-induced tyrosine phosphorylation in TLR4.
[Mh] Termos MeSH primário: Mediadores da Inflamação/metabolismo
Glicoproteínas de Membrana/metabolismo
Fator 88 de Diferenciação Mieloide/metabolismo
Receptores de Interleucina-1/metabolismo
Receptor 4 Toll-Like/metabolismo
Quinases da Família src/metabolismo
[Mh] Termos MeSH secundário: Animais
Células HEK293
Seres Humanos
Inflamação/induzido quimicamente
Inflamação/metabolismo
Lipopolissacarídeos/toxicidade
Camundongos
Fosforilação/efeitos dos fármacos
Fosforilação/fisiologia
Células RAW 264.7
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Lipopolysaccharides); 0 (Membrane Glycoproteins); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (Receptors, Interleukin-1); 0 (TIRAP protein, mouse); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  7 / 3753 MEDLINE  
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[PMID]:29289488
[Au] Autor:Lee W; Hwang MH; Lee Y; Bae JS
[Ad] Endereço:College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, BK21 Plus KNU Multi-Omics Based Creative Drug Research Team, Kyungpook National University, Daegu, 41566, Republic of Korea; Aging Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Repu
[Ti] Título:Protective effects of zingerone on lipopolysaccharide-induced hepatic failure through the modulation of inflammatory pathways.
[So] Source:Chem Biol Interact;281:106-110, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the effects of zingerone (ZGR) on lipopolysaccharide (LPS)-induced liver failure in mice, and to elucidate underlying mechanisms. ZGR is a phenolic alkanone isolated from ginger, and has potential health benefits. Mice were treated intravenously with ZGR at 12 h after LPS treatment. LPS significantly increased mortality, serum levels of alanine transaminase, aspartate transaminase, and inflammatory cytokines, and toll-like receptor 4 (TLR4) protein expression; these effects of LPS were inhibited by ZGR. It also attenuated the LPS-induced activation of myeloid differentiation primary response gene 88 and TLR-associated activator of interferon-dependent signaling pathways of the TLR system. Our results suggest that ZGR protects against LPS-induced liver damage by inhibiting the TLR-mediated inflammatory pathway, indicating its potential to treat liver diseases.
[Mh] Termos MeSH primário: Guaiacol/análogos & derivados
Falência Hepática Aguda/prevenção & controle
Fígado/efeitos dos fármacos
Substâncias Protetoras/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Citocinas/sangue
Ensaio de Imunoadsorção Enzimática
Guaiacol/administração & dosagem
Guaiacol/farmacologia
Injeções Intravenosas
Lipopolissacarídeos/toxicidade
Fígado/metabolismo
Fígado/patologia
Falência Hepática Aguda/induzido quimicamente
Falência Hepática Aguda/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fator 88 de Diferenciação Mieloide/metabolismo
Substâncias Protetoras/administração & dosagem
Receptor 4 Toll-Like/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Lipopolysaccharides); 0 (Myeloid Differentiation Factor 88); 0 (Protective Agents); 0 (Toll-Like Receptor 4); 4MMW850892 (zingerone); 6JKA7MAH9C (Guaiacol); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


  8 / 3753 MEDLINE  
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[PMID]:28747343
[Au] Autor:Savage AK; Liang HE; Locksley RM
[Ad] Endereço:Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158.
[Ti] Título:The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine.
[So] Source:J Immunol;199(5):1912-1922, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group 3 innate lymphoid cells (ILC3s) are important for intestinal health, particularly in controlling inflammation in response to epithelial dysregulation, but their role during homeostasis remains less well understood. We generated IL-22 reporter mice to assess production of this key cytokine by ILC3s in the small intestine during development and under basal conditions. Although IL-22 is produced by a variety of lymphocyte populations, constitutively high IL-22 expression was limited to lymphoid-tissue inducer (LTi) cells residing in lymph node-like structures in the gut called solitary intestinal lymphoid tissues (SILT). Constitutive IL-22 expression was dependent on the microbiota and MyD88 signaling, appeared upon weaning, and was present across the spectrum of SILT, including in cryptopatches. Activated SILT LTi cells colocalized with a rare subpopulation of activated macrophages constitutively positive for IL-12/23 p40 and capable of activating neonatal LTi cells in response to TLR stimulus. Thus, weaning leads to the organization of innate immune activation hubs at SILT that mature and are continuously sustained by signals from the microbiota. This functional and anatomic organization constitutes a significant portion of the steady-state IL-23/IL-22 axis.
[Mh] Termos MeSH primário: Interleucinas/metabolismo
Intestino Delgado/imunologia
Linfócitos/imunologia
Macrófagos/imunologia
Estruturas Linfoides Terciárias/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Imunidade Inata
Interleucina-12/metabolismo
Interleucina-23/metabolismo
Interleucinas/genética
Intestino Delgado/anatomia & histologia
Ativação Linfocitária
Linfócitos/citologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microbiota/imunologia
Fator 88 de Diferenciação Mieloide/metabolismo
Transdução de Sinais
Estruturas Linfoides Terciárias/patologia
[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-23); 0 (Interleukins); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (interleukin-22); 187348-17-0 (Interleukin-12)
[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.1700155


  9 / 3753 MEDLINE  
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[PMID]:28461572
[Au] Autor:Upadhyay K; Park JE; Yoon TW; Halder P; Kim YI; Metcalfe V; Talati AJ; English BK; Yi AK
[Ad] Endereço:Department of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163.
[Ti] Título:Group B Streptococci Induce Proinflammatory Responses via a Protein Kinase D1-Dependent Pathway.
[So] Source:J Immunol;198(11):4448-4457, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group B streptococci (GBS) are one of the leading causes of life-threatening illness in neonates. Proinflammatory responses to GBS mediated through host innate immune receptors play a critical role in the disease manifestation. However, the mechanisms involved in proinflammatory responses against GBS, as well as the contribution of signaling modulators involved in host immune defense, have not been fully elucidated. In the present study, we investigated the role of protein kinase D (PKD)1 in the proinflammatory responses to GBS. We found that both live and antibiotic-killed GBS induce activation of PKD1 through a pathway that is dependent on the TLR signaling adaptor MyD88 and its downstream kinase IL-1R-associated kinase 1, but independent of TNFR-associated factor 6. Our studies using pharmacological PKD inhibitors and PKD1-knockdown macrophages revealed that PKD1 is indispensable for GBS-mediated activation of MAPKs and NF-κB and subsequent expression of proinflammatory mediators. Furthermore, systemic administration of a PKD inhibitor protects d-galactosamine-sensitized mice from shock-mediated death caused by antibiotic-killed GBS. These findings imply that PKD1 plays a critical regulatory role in GBS-induced proinflammatory reactions and sepsis, and inhibition of PKD1 activation together with antibiotic treatment in GBS-infected neonates could be an effective way to control GBS diseases.
[Mh] Termos MeSH primário: Inflamação/imunologia
Proteína Quinase C/metabolismo
Infecções Estreptocócicas/imunologia
Infecções Estreptocócicas/metabolismo
Streptococcus agalactiae/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Recém-Nascido
Proteína Antagonista do Receptor de Interleucina 1/imunologia
Proteína Antagonista do Receptor de Interleucina 1/metabolismo
Macrófagos/imunologia
Macrófagos/microbiologia
Camundongos
Fator 88 de Diferenciação Mieloide
NF-kappa B/metabolismo
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/deficiência
Sepse/microbiologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Il1rn protein, mouse); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Myeloid Differentiation Factor 88); 0 (NF-kappa B); 0 (Tumor Necrosis Factor-alpha); EC 2.7.10.- (protein kinase D); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601089


  10 / 3753 MEDLINE  
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[PMID]:29179209
[Au] Autor:Tao Y; Wang Y; Wang X; Wang C; Bao K; Ji L; Jiang G; Hong M
[Ad] Endereço:Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China.
[Ti] Título:Calycosin Suppresses Epithelial Derived Initiative Key Factors and Maintains Epithelial Barrier in Allergic Inflammation via TLR4 Mediated NF-κB Pathway.
[So] Source:Cell Physiol Biochem;44(3):1106-1119, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Calycosin is a bioactive component of Astragali Radix, a Chinese herb for treating allergy. We have previously demonstrated that calycosin effectively inhibited allergic inflammation efficiently. The aim of this study was to explore the mechanism of calycosin on epithelial cells in allergic inflammation. METHODS: An initial stage of atopic dermatitis (AD) model in which mice were just sensitized with FITC, was established in vivo and immortalized human keratinocytes (HaCaT cells) were utilized in vitro. Initiative key cytokines, TSLP and IL-33, were measured by ELISA, qPCR, immunofluorescence and Western blot. The junctions in epithelial cells were observed by electron microscopy and tight junctions (TJs) (Occludin and ZO-1) were assessed by Western blot and immunofluorescence. TLR4, MyD88, TAK1, TIRAP and NF-κB were measured by qPCR or Western blot. RESULTS: The results showed that TSLP and IL-33 were inhibited significantly by calycosin in the initial stage of AD model. Simultaneously, calycosin attenuated the separated gap among the epithelial cells and increased the expression of TJs. TSLP/IL-33 and TJs were similarly affected in LPS-stimulated HaCaT cells in vitro. Meanwhile, calycosin not only inhibited the expressions of TLR4, MyD88, TAK1 and TIRAP, but also reduced NF-κB activation in vitro and in vivo. An NF-κB inhibitor enhanced the expressions of TJs and reduced that of TSLP/IL-33 in LPS-stimulated HaCaT cells. CONCLUSION: These results indicated that calycosin reduced the secretion of TSLP/IL-33 and attenuated the disruption of epithelial TJs by inhibiting TLR4 mediated NF-κB signaling pathway. These findings help to understand the beneficial effects of calycosin on AD, and to develop effective preventive or therapeutic strategies to combat this disease and other epithelial barrier deletion-mediated allergic diseases.
[Mh] Termos MeSH primário: Isoflavonas/farmacologia
NF-kappa B/metabolismo
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Linhagem Celular
Citocinas/análise
Citocinas/metabolismo
Dermatite Atópica/metabolismo
Dermatite Atópica/patologia
Dermatite Atópica/veterinária
Medicamentos de Ervas Chinesas/química
Medicamentos de Ervas Chinesas/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Interleucina-33/análise
Interleucina-33/metabolismo
Isoflavonas/química
Isoflavonas/metabolismo
Lipopolissacarídeos/toxicidade
MAP Quinase Quinase Quinases/genética
MAP Quinase Quinase Quinases/metabolismo
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Microscopia Eletrônica
Microscopia de Fluorescência
Simulação de Acoplamento Molecular
Fator 88 de Diferenciação Mieloide/genética
Fator 88 de Diferenciação Mieloide/metabolismo
Receptores de Interleucina-1/genética
Receptores de Interleucina-1/metabolismo
Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Drugs, Chinese Herbal); 0 (Interleukin-33); 0 (Isoflavones); 0 (Lipopolysaccharides); 0 (Membrane Glycoproteins); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (NF-kappa B); 0 (Receptors, Interleukin-1); 0 (TIRAP protein, mouse); 0 (Toll-Like Receptor 4); 0 (thymic stromal lymphopoietin); 09N3E8P7TA (7,3'-dihydroxy-4'-methoxyisoflavone); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485416



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