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  1 / 4498 MEDLINE  
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[PMID]:28456536
[Au] Autor:More Bayona JA; Karuppannan AK; Barreda DR
[Ad] Endereço:Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2P5, Canada.
[Ti] Título:Contribution of leukocytes to the induction and resolution of the acute inflammatory response in chickens.
[So] Source:Dev Comp Immunol;74:167-177, 2017 Sep.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A successful immune response against invading pathogens relies on the efficient activation of host defense mechanisms and a timely return to immune homeostasis. Despite their importance, these mechanisms remain ill-defined in most animal groups. This study focuses on the acute inflammatory response of chickens, important both as an avian model with a unique position in evolution as well as an increasingly notable target of infectious zoonotic diseases. We took advantage of an in vivo self-resolving intra-abdominal challenge model to provide an integrative view of leukocyte responses during the induction and resolution phases of acute inflammation. Our results showed rapid leukocyte infiltration into the abdominal cavity post zymosan challenge (significant increase as early as 4 h), which was dominated by heterophils. Peak leukocyte infiltration and ROS production reached maximum levels at 12 h post challenge, which was significantly earlier than comparative studies in teleost fish and mice. Both heterophils and monocyte/macrophages contributed to ROS production. Local leukocyte infiltration was preceded by an increase in peripheral leukocytes and a drop in the number of bone marrow leukocytes. The proportion of apoptotic leukocytes increased following peak of acute inflammation, rising to significant levels within the abdominal cavity by 48 h, consistent with other indicators for the resolution of inflammation. Importantly, comparison of chicken phagocytic responses with those previously shown in agnathan, teleost and murine models suggested a progressive evolutionary shift towards an increased sensitivity to pro-inflammatory pathogen-derived particles and decreased sensitivity towards homeostatic stimuli. Thus, while significant conservation can be noted across the immune systems of endotherms, this study highlights additional unique features that govern the induction and resolution of acute inflammation in the avian system, which may be relevant to disease susceptibility and performance.
[Mh] Termos MeSH primário: Doenças das Aves/imunologia
Galinhas/imunologia
Inflamação/imunologia
Leucócitos/imunologia
Peritônio/fisiologia
Zoonoses/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Apoptose
Evolução Biológica
Movimento Celular
Proliferação Celular
Peixes
Seres Humanos
Imunidade Inata
Camundongos
Fagocitose
Fisiologia Comparada
Espécies Reativas de Oxigênio/metabolismo
Zimosan/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 9010-72-4 (Zymosan)
[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:170501
[St] Status:MEDLINE


  2 / 4498 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


  3 / 4498 MEDLINE  
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[PMID]:27774606
[Au] Autor:Vallières F; Girard D
[Ad] Endereço:Laboratoire de recherche en inflammation et physiologie des granulocytes, Université du Québec, INRS-Institut Armand-Frappier, Laval, QC, Canada.
[Ti] Título:Mechanism involved in interleukin-21-induced phagocytosis in human monocytes and macrophages.
[So] Source:Clin Exp Immunol;187(2):294-303, 2017 Feb.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The interleukin (IL)-21/IL-21 receptor (R) is a promising system to be exploited for the development of therapeutic strategies. Although the biological activities of IL-21 and its cell signalling events have been largely studied in immunocytes, its interaction with human monocytes and macrophages have been neglected. Previously, we reported that IL-21 enhances Fc gamma receptor (FcRγ)-mediated phagocytosis in human monocytes and in human monocyte-derived macrophages (HMDM) and identified Syk as a novel molecular target of IL-21. Here, we elucidate further how IL-21 promotes phagocytosis in these cells. Unlike its ability to enhance phagocytosis of opsonized sheep red blood cells (SRBCs), IL-21 did not promote phagocytosis of Escherichia coli and zymosan by monocytes and did not alter the cell surface expression of CD16, CD32 and CD64. In HMDM, IL-21 was found to enhance phagocytosis of zymosan. In addition, we found that IL-21 activates p38, protein kinase B (Akt), signal transducer and activator of transcription (STAT)-1 and STAT-3 in monocytes and HMDM. Using a pharmacological approach, we demonstrate that IL-21 enhances phagocytosis by activating some mitogen-activated protein kinases (MAPKs) and phosphoinositide 3-kinase (PI3K)-Akt and Janus kinase (JAK)-STAT pathways. These results obtained in human monocytes and macrophages have to be considered for a better exploitation of the IL-21/IL-21R system for therapeutic purposes.
[Mh] Termos MeSH primário: Escherichia coli/imunologia
Interleucinas/metabolismo
Macrófagos/imunologia
Fagocitose
Receptores de Interleucina-21/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Células Cultivadas
Eritrócitos/imunologia
Seres Humanos
Interleucinas/imunologia
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Zimosan/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukins); 0 (Receptors, Interleukin-21); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (interleukin-21); 9010-72-4 (Zymosan); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12886


  4 / 4498 MEDLINE  
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[PMID]:28922655
[Au] Autor:Du J; Cheng Y; Dong S; Zhang P; Guo J; Han J; Gao F; Zhao H; Sun D; Cui J; Cai J; Liu C
[Ti] Título:Zymosan-a Protects the Hematopoietic System from Radiation-Induced Damage by Targeting TLR2 Signaling Pathway.
[So] Source:Cell Physiol Biochem;43(2):457-464, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The hematopoietic system is vulnerable to ionizing radiation and is often severely damaged by radiation. Molecules affecting radioresistance include Toll-like receptor 2. We investigated whether Zymosan-A, a novel TLR2 agonist, can protect the hematopoietic system from radiation-induced damage after total body irradiation. METHODS: Mice were exposed to total body radiation after treatment with Zymosan-A or normal saline, and their survival was recorded. Tissue damage was evaluated by hematoxylin-eosin staining. The number of nucleated cells in bone marrow was determined by flow cytometry. Cell viability and apoptosis assay were determined by CCK-8 assay and flow cytometry assay. Enzyme-linked immunosorbent assay was used to detect the level of cytokines. RESULTS: Zymosan-A protected mice from radiation-induced death and prevented radiation-induced hematopoietic system damage. Zymosan-A also promoted cell viability and inhibited cell apoptosis caused by radiation, induced radioprotective effects via TLR2, upregulated IL-6, IL-11, IL-12, and TNF-α in vivo. CONCLUSION: Zymosan-A can provide protection against radiation-induced hematopoietic system damage by targeting the TLR2 signaling pathway. Thus, Zymosan-A can be potentially effective radioprotectant.
[Mh] Termos MeSH primário: Sistema Hematopoético/efeitos dos fármacos
Sistema Hematopoético/efeitos da radiação
Protetores contra Radiação/farmacologia
Receptor 2 Toll-Like/metabolismo
Zimosan/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Linhagem Celular
Sistema Hematopoético/patologia
Masculino
Camundongos Endogâmicos C57BL
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Radiation-Protective Agents); 0 (Toll-Like Receptor 2); 9010-72-4 (Zymosan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1159/000480472


  5 / 4498 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


  6 / 4498 MEDLINE  
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[PMID]:28674178
[Au] Autor:Aswad M; Assi S; Schif-Zuck S; Ariel A
[Ad] Endereço:Department of Biology, Faculty of Natural Sciences, University of Haifa, Haifa 3498838, Israel; and.
[Ti] Título:CCL5 Promotes Resolution-Phase Macrophage Reprogramming in Concert with the Atypical Chemokine Receptor D6 and Apoptotic Polymorphonuclear Cells.
[So] Source:J Immunol;199(4):1393-1404, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The engulfment of apoptotic polymorphonuclear cells (PMN) during the resolution of inflammation leads to macrophage reprogramming culminating in reduced proinflammatory and increased anti-inflammatory mediator secretion. The atypical chemokine receptor D6/ACKR2 is expressed on apoptotic PMN and plays an important role in regulating macrophage properties during and after engulfment. In this study, we found that the inflammatory chemokine CCL5 is mostly retained (75%) during the resolution of zymosan A peritonitis in mice. Moreover, this chemokine is secreted by resolution-phase macrophages (2.5 ng/ml) and promotes their reprogramming in vivo in D6 mice (2-fold increase in IL-10/IL-12 ratio) but not their D6 counterparts. In addition, CCL5 enhanced macrophage reprogramming ex vivo exclusively when bound to D6 apoptotic PMN. Signaling through p38MAPK and JNK in reprogrammed macrophages was enhanced by CCL5-bound apoptotic PMN (3.6-4 fold) in a D6-dependent manner, and was essential for reprogramming. Thus, CCL5 exerts a novel proresolving role on macrophages when acting in concert with apoptotic PMN-expressed D6.
[Mh] Termos MeSH primário: Apoptose
Quimiocina CCL5/imunologia
Quimiocina CCL5/metabolismo
Macrófagos/fisiologia
Neutrófilos/imunologia
Peritonite/imunologia
Receptores CCR10/metabolismo
[Mh] Termos MeSH secundário: Animais
Quimiocina CCL5/farmacologia
Regulação da Expressão Gênica
Inflamação/metabolismo
Macrófagos/imunologia
Camundongos
Peritonite/induzido quimicamente
Ligação Proteica
Receptores CCR10/genética
Receptores CCR10/imunologia
Zimosan/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl5 protein, mouse); 0 (Chemokine CCL5); 0 (Receptors, CCR10); 0 (chemokine receptor D6); 9010-72-4 (Zymosan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1502542


  7 / 4498 MEDLINE  
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[PMID]:28412994
[Au] Autor:Alheiros-Lira MC; Jurema-Santos GC; da-Silva HT; da-Silva AC; Moreno Senna S; Ferreira E Silva WT; Ferraz JC; Leandro CG
[Ad] Endereço:1Department of Nutrition,Federal University of Pernambuco,Recife, 50670-901, Brazil.
[Ti] Título:Effects of high-fat diet on somatic growth, metabolic parameters and function of peritoneal macrophages of young rats submitted to a maternal low-protein diet.
[So] Source:Br J Nutr;117(6):796-803, 2017 Mar.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study evaluated the effects of a post-weaning high-fat (HF) diet on somatic growth, food consumption, metabolic parameters, phagocytic rate and nitric oxide (NO) production of peritoneal macrophages in young rats submitted to a maternal low-protein (LP) diet. Male Wistar rats (aged 60 d) were divided in two groups (n 22/each) according to their maternal diet during gestation and lactation: control (C, dams fed 17 % casein) and LP (dams fed 8 % casein). At weaning, half of the groups were fed HF diet and two more groups were formed (HF and low protein-high fat (LP-HF)). Somatic growth, food and energy intake, fat depots, serum glucose, cholesterol and leptin concentrations were evaluated. Phagocytic rate and NO production were analysed in peritoneal macrophages under stimulation of zymosan and lipopolysaccharide (LPS)+interferon γ (IFN-γ), respectively. The maternal LP diet altered the somatic parameters of growth and development of pups. LP and LP-HF pups showed a higher body weight gain and food intake than C pups. HF and LP-HF pups showed increased retroperitoneal and epididymal fat depots, serum level of TAG and total cholesterol compared with C and LP pups. After LPS+IFN-γ stimulation, LP and LP-HF pups showed reduced NO production when compared with their pairs. Increased phagocytic activity and NO production were seen in LP but not LP-HF peritoneal macrophages. However, peritoneal macrophages of LP pups were hyporesponsive to LPS+IFN-γ induced NO release, even after a post-weaning HF diet. Our data demonstrated that there was an immunomodulation related to dietary fatty acids after the maternal LP diet-induced metabolic programming.
[Mh] Termos MeSH primário: Dieta Hiperlipídica
Dieta com Restrição de Proteínas
Gorduras na Dieta/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Desnutrição/complicações
Fenômenos Fisiológicos da Nutrição Materna
Ganho de Peso
[Mh] Termos MeSH secundário: Animais
Gorduras na Dieta/administração & dosagem
Ingestão de Energia/efeitos dos fármacos
Feminino
Interferon gama/sangue
Lactação
Lipopolissacarídeos
Macrófagos Peritoneais/metabolismo
Masculino
Óxido Nítrico/metabolismo
Obesidade/etiologia
Obesidade/imunologia
Obesidade/metabolismo
Gravidez
Complicações na Gravidez
Efeitos Tardios da Exposição Pré-Natal
Ratos Wistar
Desmame
Zimosan
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Lipopolysaccharides); 31C4KY9ESH (Nitric Oxide); 82115-62-6 (Interferon-gamma); 9010-72-4 (Zymosan)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517000708


  8 / 4498 MEDLINE  
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[PMID]:28382433
[Au] Autor:Dos Anjos LMJ; da Fonseca AS; Gameiro J; de Paoli F
[Ad] Endereço:Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Juiz de Fora, Rua José Lourenço Kelmer, s/n-Campus Universitário, São Pedro, Juiz de Fora, Minas Gerais, 36036900, Brazil. luciamara.anjos@ufjf.edu.br.
[Ti] Título:Apoptosis induced by low-level laser in polymorphonuclear cells of acute joint inflammation: comparative analysis of two energy densities.
[So] Source:Lasers Med Sci;32(5):975-983, 2017 Jul.
[Is] ISSN:1435-604X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anti-inflammatory property of low-level laser therapy (LLLT) has been widely described in literature, although action mechanisms are not always clarified. Thus, this study aimed to evaluate apoptosis mechanisms in the LLLT anti-inflammatory effects on the arthritis experimental model in vivo at two different energy densities (3 and 30 Jcm ). Arthritis was induced in mice by zymosan solution, animals were distributed into five groups, and morphological analysis, immunocytochemistry and gene expressions for apoptotic proteins were performed. Data showed an anti-inflammatory effect, DNA fragmentation in polymorphonuclear (PMN) cells and alteration in gene expression of proteins related to apoptosis pathways after LLLT. p53 gene expression increased at both energy densities, Bcl2 gene expression increased at 3 Jcm , and Bcl2 tissue expression decreased at 30 Jcm . In addition, apoptosis was restricted to PMN cells. Results suggest that apoptosis in PMN cells comprise part of LLLT anti-inflammatory mechanisms by disbalance promotion between expression of pro-apoptotic (Bax and p53) and anti-apoptotic (Bcl-2) proteins, with pro-apoptotic gene expression selectively in PMN cells.
[Mh] Termos MeSH primário: Apoptose/efeitos da radiação
Inflamação/patologia
Articulações/patologia
Terapia com Luz de Baixa Intensidade
Neutrófilos/patologia
Neutrófilos/efeitos da radiação
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Artrite Experimental/genética
Artrite Experimental/patologia
Artrite Experimental/radioterapia
Fragmentação do DNA/efeitos da radiação
Regulação da Expressão Gênica/efeitos da radiação
Inflamação/genética
Masculino
Camundongos Endogâmicos C57BL
Neutrófilos/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Zimosan
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Messenger); 9010-72-4 (Zymosan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1007/s10103-017-2196-8


  9 / 4498 MEDLINE  
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[PMID]:28366510
[Au] Autor:Riedemann NC; Habel M; Ziereisen J; Hermann M; Schneider C; Wehling C; Kirschfink M; Kentouche K; Guo R
[Ad] Endereço:InflaRx GmbH, Jena, Germany. Electronic address: Niels.Riedemann@inflarx.de.
[Ti] Título:Controlling the anaphylatoxin C5a in diseases requires a specifically targeted inhibition.
[So] Source:Clin Immunol;180:25-32, 2017 Jul.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The terminal complement split product C5a has been described as an important mediator in inflammatory diseases. C5a is generated upon cleavage of C5 and earlier research suggests that, besides the known C5 convertases formed upon activation of the complement pathways, various enzymes could activate C5 directly. We demonstrate that eculizumab effectively blocks C5 activation when mediated by C5-convertase formation, but fails to block C5a generation resulting from direct enzymatic cleavage by trypsin and thrombin. C5a generated by these enzymes is shown to be fully biologically functional and can be blocked by IFX-1, a specific monoclonal anti-human C5a antibody. We further report clinical cases of atypical hemolytic uremic syndrome (aHUS) and C3 Glomerulonephritis (C3GN) patients under treatment with eculizumab presenting substantially elevated C5a levels. Thus, blocking the C5 convertase mediated activation of C5 may not be efficient to control C5a-mediated effects in human disease and that a targeted approach is warranted.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/farmacologia
Síndrome Hemolítico-Urêmica Atípica/imunologia
Complemento C5a/imunologia
Glomerulonefrite/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/uso terapêutico
Síndrome Hemolítico-Urêmica Atípica/tratamento farmacológico
Convertases de Complemento C3-C5/imunologia
Glomerulonefrite/tratamento farmacológico
Seres Humanos
Trombina/imunologia
Tripsina/imunologia
Zimosan/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 80295-54-1 (Complement C5a); 9010-72-4 (Zymosan); A3ULP0F556 (eculizumab); EC 3.4.21.- (Complement C3-C5 Convertases); EC 3.4.21.4 (Trypsin); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE


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[PMID]:27766379
[Au] Autor:Mogilski S; Kubacka M; Lazewska D; Wiecek M; Gluch-Lutwin M; Tyszka-Czochara M; Bukowska-Strakova K; Filipek B; Kiec-Kononowicz K
[Ad] Endereço:Departament of Pharmacodynamics, Jagiellonian University Medical College, Medyczna 9, 30-688, Kraków, Poland. szczepan.mogilski@uj.edu.pl.
[Ti] Título:Aryl-1,3,5-triazine ligands of histamine H receptor attenuate inflammatory and nociceptive response to carrageen, zymosan and lipopolysaccharide.
[So] Source:Inflamm Res;66(1):79-95, 2017 Jan.
[Is] ISSN:1420-908X
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE AND DESIGN: Histamine H receptor (H R) offers a great potential for new therapeutic strategies for the treatment of inflammation-based diseases. The aim of this study is to present the pharmacological profile of two recently synthesized ligands of H R with particular reference to their anti-inflammatory and analgesic activity. MATERIALS AND SUBJECTS: We used mice and rats in the in vivo tests. We also used murine RAW 264.7 cells and isolated guinea-pig ileum in in vitro test. TREATMENTS: In the in vivo tests, animals were pre-treated with the increasing doses of investigated compounds (12.5, 25 and 50 mg/kg) and reference compounds: JNJ7777120 (25 mg/kg), indomethacin (10 mg/kg). Macrophages were pre-treated with two concentrations of tested compounds 100 and 10 µM. METHODS: We examined anti-inflammatory and analgesic effects of the new H R antagonists in the in vivo models of inflammation induced by carrageenan or zymosan. We assessed the level of cAMP and release of cytokines, ROS and NO in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Moreover, we assessed the affinity of the investigated compounds for histamine H receptor in functional studies. RESULTS: Both investigated compounds reduced paw edema, mechanical and thermal hyperalgesia in the carrageenan-induced acute inflammation. Moreover, administration of the investigated compounds resulted in decreased granulocyte influx and attenuated nociceptive reaction in the zymosan-induced peritonitis model. In the same model of inflammation, the investigated compounds reduced vascular permeability; however, this effect was observed only after the highest applied dose. Furthermore, the test compounds had no impact on cell viability in the experiments on RAW 264.7 macrophages. In these cells, stimulated with LPS, the test compounds decreased reactive oxygen species (ROS) production. They increased the cellular concentration of cAMP and attenuated the production of inflammatory cytokines such as TNFα and IL-1ß. All results were comparable to those obtained for the reference compound JNJ7777120 with the exception of the impact on NO production. Nevertheless, this effect was similar to that obtained for the other reference compound rolipram, which is a phosphodiesterase 4 (PDE 4) inhibitor. Further experiments revealed that both of the investigated compounds possessed relatively low affinity for histamine H receptor and do not inhibit the activity of the PDE 4B1 enzyme. In addition, all the effects of the investigated compounds in in vivo experiments were observed at doses that did not cause neurologic deficits in rotarod test and did not reduce spontaneous locomotor activity. CONCLUSIONS: Our results demonstrate the anti-inflammatory and analgesic activity of the new aryl-1,3,5-triazine derivatives, which are primarily H R-dependent.
[Mh] Termos MeSH primário: Analgésicos/uso terapêutico
Anti-Inflamatórios/uso terapêutico
Antagonistas dos Receptores Histamínicos/uso terapêutico
Triazinas/uso terapêutico
[Mh] Termos MeSH secundário: Analgésicos/farmacologia
Animais
Anti-Inflamatórios/farmacologia
Carragenina
AMP Cíclico/metabolismo
Cobaias
Antagonistas dos Receptores Histamínicos/farmacologia
Hiperalgesia/induzido quimicamente
Hiperalgesia/tratamento farmacológico
Hiperalgesia/metabolismo
Inflamação/induzido quimicamente
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Interleucina-1beta/metabolismo
Ligantes
Lipopolissacarídeos
Masculino
Camundongos
Óxido Nítrico/metabolismo
Dor/induzido quimicamente
Dor/tratamento farmacológico
Dor/metabolismo
Células RAW 264.7
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
Receptores Histamínicos/metabolismo
Triazinas/farmacologia
Fator de Necrose Tumoral alfa/metabolismo
Zimosan
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Anti-Inflammatory Agents); 0 (Histamine Antagonists); 0 (Interleukin-1beta); 0 (Ligands); 0 (Lipopolysaccharides); 0 (Reactive Oxygen Species); 0 (Receptors, Histamine); 0 (Triazines); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); 9000-07-1 (Carrageenan); 9010-72-4 (Zymosan); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE
[do] DOI:10.1007/s00011-016-0997-z



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