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  1 / 23653 MEDLINE  
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[PMID]:29324883
[Au] Autor:Jenny L; Dobó J; Gál P; Pál G; Lam WA; Schroeder V
[Ad] Endereço:Experimental Haemostasis Group, Department for BioMedical Research, University of Bern, Bern, Switzerland.
[Ti] Título:MASP-1 of the complement system enhances clot formation in a microvascular whole blood flow model.
[So] Source:PLoS One;13(1):e0191292, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The complement and coagulation systems closely interact with each other. These interactions are believed to contribute to the proinflammatory and prothrombotic environment involved in the development of thrombotic complications in many diseases. Complement MASP-1 (mannan-binding lectin-associated serine protease-1) activates coagulation factors and promotes clot formation. However, this was mainly shown in purified or plasma-based static systems. Here we describe the role of MASP-1 and complement activation in fibrin clot formation in a microvascular, whole blood flow model. This microfluidic system simulates blood flow through microvessels at physiological flow and shear rates and represents the closest model system to human physiology so far. It features parallel microchannels cultured with endothelial cells in a transparent microfluidic chip allowing real-time evaluation of clot formation by confocal microscopy. To test their effects on clot formation, we added the following activators or inhibitors (individually or in combination) to whole blood and performed perfusion experiments: rMASP-1cf (recombinant active form of MASP-1), complement activator zymosan, selective MASP-1 inhibitor SGMI-1 (based on the Schistocerca gregaria protease inhibitor scaffold), classical pathway inhibitor rSALO (recombinant salivary anti-complement from Lutzomyia longipalpis). Addition of rMASP-1cf resulted in accelerated fibrin clot formation while addition of SGMI-1 delayed it. Complement activation by zymosan led to increased clot formation and this effect was partially reversed by addition of rSALO and almost abolished in combination with SGMI-1. We show for the first time a strong influence of MASP-1, complement activation and pathway-specific inhibition on coagulation in a microvascular flow system that is closest to human physiology, further underpinning the in vivo relevance of coagulation and complement interactions.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Proteínas do Sistema Complemento/metabolismo
Serina Proteases Associadas a Proteína de Ligação a Manose/metabolismo
Microvasos/fisiologia
[Mh] Termos MeSH secundário: Seres Humanos
Lectinas/metabolismo
Serina Proteases Associadas a Proteína de Ligação a Manose/química
Domínios Proteicos
Zimosan/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lectins); 9007-36-7 (Complement System Proteins); 9010-72-4 (Zymosan); EC 3.4.21.- (MASP1 protein, human); EC 3.4.21.- (Mannose-Binding Protein-Associated Serine Proteases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191292


  2 / 23653 MEDLINE  
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[PMID]:29308852
[Au] Autor:Demyanova KA; Kozlovskaya NL; Bobrova LA; Kozlov LV; Andina SS; Yurova VA; Kuchieva AM; Roshchupkina SV; Shilov EM
[Ti] Título:Complement System Abnormalities in Patients with Atypical Hemolytic Uremic Syndrome and Catastrophic Antiphospholipid Syndrome.
[So] Source:Vestn Ross Akad Med Nauk;72(1):42-52, 2017.
[Is] ISSN:0869-6047
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:Background: The role of the alternative complement pathway (AP) abnormalities in the pathogenesis of aHUS is well studied. Clinical and morphological manifestations of atypical HUS and catastrophic APS are often similar. However, studies on the state of AP in patients with CAPS are virtually absent. Aims: The aim of our study was to assess the state of AP in patients with CAPS and aHUS. Patients and methods: The study enrolled 67 patients (pts) with a diagnosis of CAPS (28 pts) and aHUS (39 pts). Studies of the complement system are made of 10 pts with CAPS and 20 aHUS. Factor H, I, B, D content, functional activity of factor H, and complement components C3, C4 was determined in serum by ELISA kit. Results: Patients with CAPS and aHUS showed similar changes in complement biomarkers. The factor H level in the serum was significantly higher than the standard value. However, the specific activity of factor H reduced, mean rate 59% for aHUS and 26% for CAPS. The median value of factor D was twice higher than the normal range in both groups, indicating the activation of the AP. Conclusions: There are indications of an AP activation not only in pts with aHUS but in CAPS pts too. We suppose that the activity of factor H is a more sensitive indicator of complement system changes than factor H level. Patients with CAPS and aHUS have similar clinical and laboratory characteristics. However, CAPS is more severe, with the involvement of a larger number of vascular beds. Perhaps this is due to the double damaging effects on the endothelium ­ of antiphospholipid antibodies (aPL) and activated complement. So we hypothesize that CAPS can be called aPL-mediated TMA in pts with a complement system defect.
[Mh] Termos MeSH primário: Síndrome Antifosfolipídica
Síndrome Hemolítico-Urêmica Atípica
Fator H do Complemento
Proteínas do Sistema Complemento
Microangiopatias Trombóticas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Anticorpos Antifosfolipídeos/sangue
Síndrome Antifosfolipídica/diagnóstico
Síndrome Antifosfolipídica/metabolismo
Síndrome Antifosfolipídica/fisiopatologia
Síndrome Hemolítico-Urêmica Atípica/diagnóstico
Síndrome Hemolítico-Urêmica Atípica/metabolismo
Síndrome Hemolítico-Urêmica Atípica/fisiopatologia
Fator H do Complemento/análise
Fator H do Complemento/metabolismo
Via Alternativa do Complemento
Proteínas do Sistema Complemento/análise
Proteínas do Sistema Complemento/metabolismo
Endotélio Vascular/metabolismo
Endotélio Vascular/fisiopatologia
Feminino
Seres Humanos
Masculino
Estatística como Assunto
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antiphospholipid); 80295-65-4 (Complement Factor H); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.15690/vramn769


  3 / 23653 MEDLINE  
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[PMID]:29266058
[Au] Autor:Lan JH; Tinckam K
[Ad] Endereço:Division of Nephrology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Título:Clinical Utility of Complement Dependent Assays in Kidney Transplantation.
[So] Source:Transplantation;102(1S Suppl 1):S14-S22, 2018 01.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Formation of antibodies against polymorphic HLA molecules on donor endothelium is central to the pathogenesis of antibody-mediated rejection, the dominant cause of long-term kidney allograft loss. Although introduction of the single-antigen bead assay has greatly facilitated the immune risk assessment of transplant recipients, it is recognized that not all IgG HLA antibodies detected using this method are equally relevant. In recent years, novel assays (C4d, C1q, C3d) have been developed to interrogate the complement-activating potential of anti-HLA antibodies in vitro, with the hypothesis that complement-fixing antibodies are more immediately injurious to the graft compared with noncomplement-binding antibodies. Although initial studies demonstrated the potential of these assays to risk-stratify antibodies beyond the conventional limited metric of mean fluorescence intensity values, new data from recent analyses challenge some of these early findings. In this review, we examine the technical aspects of these assays and key studies that evaluated the discriminant capacity of these tests to predict numerous outcomes in kidney transplantation. We discuss conflicting data and emerging controversies in the context of recent experimental evidence which offer new insights into the major factors that influence complement activation. Finally, we provide our perspective on the current role and utility of complement diagnostic assays as 1 variable in the multifactorial risk assessment and management of kidney transplant recipients.
[Mh] Termos MeSH primário: Ativação do Complemento/imunologia
Proteínas do Sistema Complemento/imunologia
Rejeição de Enxerto/imunologia
Antígenos HLA/imunologia
Teste de Histocompatibilidade/métodos
Isoanticorpos/metabolismo
Transplante de Rim
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Rejeição de Enxerto/prevenção & controle
Seres Humanos
Isoanticorpos/imunologia
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (HLA Antigens); 0 (Isoantibodies); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001819


  4 / 23653 MEDLINE  
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[PMID]:29199277
[Au] Autor:Ricklin D; Mastellos DC; Reis ES; Lambris JD
[Ad] Endereço:Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland.
[Ti] Título:The renaissance of complement therapeutics.
[So] Source:Nat Rev Nephrol;14(1):26-47, 2018 Jan.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The increasing number of clinical conditions that involve a pathological contribution from the complement system - many of which affect the kidneys - has spurred a regained interest in therapeutic options to modulate this host defence pathway. Molecular insight, technological advances, and the first decade of clinical experience with the complement-specific drug eculizumab, have contributed to a growing confidence in therapeutic complement inhibition. More than 20 candidate drugs that target various stages of the complement cascade are currently being evaluated in clinical trials, and additional agents are in preclinical development. Such diversity is clearly needed in view of the complex and distinct involvement of complement in a wide range of clinical conditions, including rare kidney disorders, transplant rejection and haemodialysis-induced inflammation. The existing drugs cannot be applied to all complement-driven diseases, and each indication has to be assessed individually. Alongside considerations concerning optimal points of intervention and economic factors, patient stratification will become essential to identify the best complement-specific therapy for each individual patient. This Review provides an overview of the therapeutic concepts, targets and candidate drugs, summarizes insights from clinical trials, and reflects on existing challenges for the development of complement therapeutics for kidney diseases and beyond.
[Mh] Termos MeSH primário: Inativadores do Complemento/uso terapêutico
Proteínas do Sistema Complemento/imunologia
Rejeição de Enxerto/tratamento farmacológico
Nefropatias/tratamento farmacológico
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/uso terapêutico
Ativação do Complemento/imunologia
Descoberta de Drogas
Seres Humanos
Inflamação
Nefropatias/imunologia
Terapia de Alvo Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Complement Inactivating Agents); 9007-36-7 (Complement System Proteins); A3ULP0F556 (eculizumab)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.156


  5 / 23653 MEDLINE  
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[PMID]:27771173
[Au] Autor:Farkas P; Csuka D; Mikes B; Sinkovits G; Réti M; Németh E; Rácz K; Madách K; Gergely M; Demeter J; Prohászka Z
[Ad] Endereço:3rd Department of Internal Medicine, Research Laboratory and Füst György Complement Diagnostic Laboratory, Semmelweis University, Budapest, Hungary.
[Ti] Título:Complement activation, inflammation and relative ADAMTS13 deficiency in secondary thrombotic microangiopathies.
[So] Source:Immunobiology;222(2):119-127, 2017 02.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The secondary forms of hemolytic uremic syndrome/thrombotic thrombocytopenic purpura (secondary TMA) emerge as complications of coexisting diseases. OBJECTIVES: We hypothesized that secondary TMA could be characterized by the presence of relative ADAMTS13 deficiency and complement activation, and this relationship may have a prognostic value for outcome. PATIENTS AND METHODS: Fifty-three patients with thrombotic microangiopathy (TMA) and coexisting disease (such as malignancies, sepsis, heart surgery with extracorporeal circulation, solid organ transplantation, systemic autoimmune disorders), 41 patient controls, and 34 healthy controls were enrolled in our case-control study with 30days follow-up. Complement profile (from serum) and activation products, von Willebrand factor (VWF, from EDTA plasma), and ADAMTS13 activity were determined. RESULTS: ADAMTS13 activity was reduced, while VWF level was elevated in secondary TMA patients. The activity of the classical, lectin and alternative pathways, as well as the levels of C3, C4, and Factor H were significantly lower in secondary TMA patients, and were accompanied by high activation product levels (C3a and sC5b-9). Factor H concentration correlated to relative ADAMTS13 deficiency (i.e. VWF/ADAMTS13 ratio (r=-0.368, p=0.019)). 28/53 patients (53%) died during the follow-up period. Increased sC5b-9, C3a, and C reactive protein levels were all associated with a poor patient outcome. CONCLUSIONS: Our results indicate that the secondary TMA syndrome and its poor outcome is characterized by relative ADAMTS13 deficiency, inflammation, and complement activation with consumption via the classical and alternative pathways. It is yet to be determined whether complement inhibition could be a possible therapeutic option for patients with secondary TMA.
[Mh] Termos MeSH primário: Proteína ADAMTS13/deficiência
Ativação do Complemento/imunologia
Proteínas do Sistema Complemento/imunologia
Inflamação/complicações
Microangiopatias Trombóticas/etiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores
Estudos de Casos e Controles
Criança
Pré-Escolar
Comorbidade
Ativação do Complemento/genética
Proteínas do Sistema Complemento/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Modelos de Riscos Proporcionais
Microangiopatias Trombóticas/diagnóstico
Microangiopatias Trombóticas/metabolismo
Microangiopatias Trombóticas/mortalidade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 9007-36-7 (Complement System Proteins); EC 3.4.24.87 (ADAMTS13 Protein)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29242207
[Au] Autor:Schmidt CQ; Verschoor A
[Ad] Endereço:ULM UNIVERSITY.
[Ti] Título:Complement and coagulation: so close, yet so far.
[So] Source:Blood;130(24):2581-2582, 2017 12 14.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Coagulação Sanguínea
Proteínas do Sistema Complemento
[Mh] Termos MeSH secundário: Ativação do Complemento
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-10-811943


  7 / 23653 MEDLINE  
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[PMID]:27775697
[Au] Autor:Dhakal P; Bhatt VR
[Ad] Endereço:Department of Medicine, Michigan State University, East Lansing, MI, USA.
[Ti] Título:Is complement blockade an acceptable therapeutic strategy for hematopoietic cell transplant-associated thrombotic microangiopathy?
[So] Source:Bone Marrow Transplant;52(3):352-356, 2017 Mar.
[Is] ISSN:1476-5365
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Diagnosis and management of hematopoietic cell transplant-associated thrombotic microangiopathy (TA-TMA) are very complex and controversial, given multiple ongoing issues and comorbidities in sick transplant recipients. Complement activation via classic and alternative pathways is emerging as a potential pathogenetic mechanism in the development of TA-TMA. Complement-centric diagnostic strategy using functional and genetic tests may possibly support diagnosis, enhance molecular understanding and direct drug development. Complement blockade using eculizumab has shown some promising rates of hematologic responses, however, survival may still be poor. Early discontinuation of calcineurin inhibitor where feasible, use of eculizumab, aggressive infection prophylaxis, close monitoring and early treatment of potential complications including GvHD and organ failure may improve outcomes. A number of complement inhibitors are in the development and may change treatment paradigm. Future studies are important to better understand TA-TMA as a disease process and may aim to confirm the role of complement activation in TA-TMA, enhance diagnostic strategy, determine therapeutic approaches and strategies to reduce the risk of other complications particularly infection and GvHD.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Ativação do Complemento/efeitos dos fármacos
Proteínas do Sistema Complemento/metabolismo
Transplante de Células-Tronco Hematopoéticas
Microangiopatias Trombóticas/tratamento farmacológico
[Mh] Termos MeSH secundário: Aloenxertos
Inibidores de Calcineurina/uso terapêutico
Doença Enxerto-Hospedeiro/tratamento farmacológico
Doença Enxerto-Hospedeiro/etiologia
Doença Enxerto-Hospedeiro/metabolismo
Seres Humanos
Controle de Infecções
Microangiopatias Trombóticas/etiologia
Microangiopatias Trombóticas/metabolismo
Microangiopatias Trombóticas/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Calcineurin Inhibitors); 9007-36-7 (Complement System Proteins); A3ULP0F556 (eculizumab)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/bmt.2016.253


  8 / 23653 MEDLINE  
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[PMID]:28745692
[Au] Autor:Yurova VA; Bobrova LA; Kozlovskaya NL; Korotchaeva YV; Serova AG; Kozlov LV; Andina SS; Demyanova KA; Kuchieva AM; Roshchupkina SV
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
[Ti] Título:[Changes in the complement system in membranoproliferative glomerulonephritis].
[Ti] Título:Izmeneniia v sisteme komplementa pri membranoproliferativnom glomerulonefrite..
[So] Source:Ter Arkh;89(6):69-77, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To compare the clinical manifestations membranoproliferative glomerulonephritis (MPGN) in its idiopathic variant, lupus nephritis (LN), and C3 glomerulopathy (C3-GP), by comparing them with changes in the complement system. SUBJECTS AND METHODS: The clinic of nephrology followed up 42 patients with different types of MPGN in 2013 to 2015. The study included 35 patients divided into 3 groups: 1) 8 patients with C3-GP, 2) 13 with idiopathic MPGN; 3) 14 with Class IV LN. The investigators studied the blood and urine levels of components and markers for activation of the classical and alternative pathways (C3 and C4, С3а, C5a, CFH, CFB, and CFD) of the terminal complement complex (TCC). RESULTS: The detection rate of C3-GP was 19%. The patients with C3-GP were noted to have the lowest blood concentration of S3 and the highest urinary level of С3а, C5a, TCC, CFH, CFB, and CFD. C3 nephritic factor was detected in 2 patients from the C3-GP (dense deposit disease) group. CONCLUSION: Alternative complement pathway dysregulation caused by genetic or autoimmune factors plays a leading role in the pathogenesis of C3-GP.
[Mh] Termos MeSH primário: Complemento C3/metabolismo
Proteínas do Sistema Complemento/metabolismo
Glomerulonefrite Membranoproliferativa
Nefrite Lúpica
[Mh] Termos MeSH secundário: Adulto
Complemento C3/urina
Proteínas do Sistema Complemento/urina
Feminino
Glomerulonefrite Membranoproliferativa/sangue
Glomerulonefrite Membranoproliferativa/urina
Seres Humanos
Nefrite Lúpica/sangue
Nefrite Lúpica/urina
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C3); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789669-77


  9 / 23653 MEDLINE  
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[PMID]:28951216
[Au] Autor:Wang H; Li N; Zhu C; Shi S; Jin H; Wang S
[Ad] Endereço:The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, Institute of Chinese Materia Medica Shanghai University of Traditional Chinese Medicine, Shanghai 201210, China.
[Ti] Título:Anti-complementary activity of two homogeneous polysaccharides from Eclipta prostrata.
[So] Source:Biochem Biophys Res Commun;493(2):887-893, 2017 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Complement-mediated inflammation and tissue damage is an important drive to pathology in autoimmune diseases, targeting inhibit the complement activation is promising treatment strategy for these diseases. We performed anticomplement activity-guided fractionation of the water extract of Eclipta prostrata by ion-exchange and size-exclusion chromatography, yielding two bioactive polysaccharides EAP20-1 and EAP20-2. The molecular weights of EAP20-1 and EAP20-2 were respectively calculated to be 5.2 kDa and 6.3 kDa by HPGPC, both polysaccharides was composed by d-Gal, l-Glc, and Ara at different ratios of 7.3:2.7:1 and 7.6:3.1:1. In addition, the main linkage types of EAP20-1 and EAP20-2 were ß-1,4-Gal, ß-1,6-Gal and α-1,4,6-Glc according to methylation analyses. EAP20-1 and EAP20-2 exhibited significant inhibitory effect on the complement activation through both classical and alternative pathways and with no influence on the coagulation system. Preliminary mechanism study indicated that both EAP20-1 and EAP20-2 inhibited the activation of the complement system by interacting with C1q, C1r, C1s, C2, C4, C5, C7, and C9 components.
[Mh] Termos MeSH primário: Ativação do Complemento/efeitos dos fármacos
Proteínas do Sistema Complemento/imunologia
Eclipta/química
Polissacarídeos/química
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Coagulação Sanguínea/efeitos dos fármacos
Cromatografia em Gel
Polissacarídeos/isolamento & purificação
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polysaccharides); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


  10 / 23653 MEDLINE  
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[PMID]:28862638
[Au] Autor:Sarlus H; Heneka MT
[Ad] Endereço:Department of Neurodegenerative Diseases and Gerontopsychiatry, University of Bonn, Bonn, Germany.
[Ti] Título:Microglia in Alzheimer's disease.
[So] Source:J Clin Invest;127(9):3240-3249, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglia are brain-resident myeloid cells that mediate key functions to support the CNS. Microglia express a wide range of receptors that act as molecular sensors, which recognize exogenous or endogenous CNS insults and initiate an immune response. In addition to their classical immune cell function, microglia act as guardians of the brain by promoting phagocytic clearance and providing trophic support to ensure tissue repair and maintain cerebral homeostasis. Conditions associated with loss of homeostasis or tissue changes induce several dynamic microglial processes, including changes of cellular morphology, surface phenotype, secretory mediators, and proliferative responses (referred to as an "activated state"). Activated microglia represent a common pathological feature of several neurodegenerative diseases, including Alzheimer's disease (AD). Cumulative evidence suggests that microglial inflammatory activity in AD is increased while microglial-mediated clearance mechanisms are compromised. Microglia are perpetually engaged in a mutual interaction with the surrounding environment in CNS; thus, diverse microglial reactions at different disease stages may open new avenues for therapeutic intervention and modification of inflammatory activities. In this Review, the role of microglia in the pathogenesis of AD and the modulation of microglia activity as a therapeutic modality will be discussed.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Microglia/fisiologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/patologia
Doença de Alzheimer/terapia
Animais
Encéfalo/metabolismo
Proliferação Celular
Sistema Nervoso Central/metabolismo
Proteínas do Sistema Complemento/metabolismo
Citocinas/metabolismo
Seres Humanos
Sistema Imunitário
Inflamação
Macrófagos/metabolismo
Macrófagos/fisiologia
Camundongos
Microglia/metabolismo
Doenças Neurodegenerativas/metabolismo
Doenças Neurodegenerativas/patologia
Doenças Neurodegenerativas/terapia
Fagocitose
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Toll-Like Receptors); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE



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