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  1 / 106 MEDLINE  
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[PMID]:29386429
[Au] Autor:Uno K
[Ad] Endereço:Faculty of Pharmacy, Chiba Institute of Science.
[Ti] Título:[Pathogenic Mechanism and Diagnostic Testing for Drug Allergies].
[So] Source:Yakugaku Zasshi;138(2):151-167, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Three stages of the pathogenic mechanism of drug allergies can be considered: antigen formation, immune reaction and inflammation/disorder reaction. Drugs are thought to form 4 types of antigens: drug only, polymers, drug-carrier conjugates, and metabolite-carrier complexes. Antigens are recognized by B cell receptors and T cell receptors. Helper T cells (Th) are differentiated into four subsets, namely, Th1, Th2, Th17 and regulatory T cells (Treg). Th1 produces interleukin (IL)-2 and interferon (IFN)-γ, and activates macrophages and cytotoxic T cells (Tc). Macrophages induce type IV allergies, and Tc lead to serious type IV allergies. On the other hand, Th2 produces IL-4, IL-5, and IL-6, etc., and activates B cells. B cells produce IgE antibodies, and the IgE antibody affects mast cells and induces type I allergies. Activated eosinophil leads to the chronic state of type I allergy. Diagnostic testing for allergenic drugs is necessary for patients with drug allergies. Because in vivo diagnostic tests for allergenic drugs are associated with a risk and burden to the patient, in vitro allergy tests are recommended to identify allergenic drugs. In allergy tests performed in vitro, cytological tests are more effective than serological tests, and the leukocyte migration test (LMT) presently has the highest efficacy. An LMT-chamber is better than LMT-agarose in terms of usability and sensitivity, and it can detect about 80% of allergenic drugs.
[Mh] Termos MeSH primário: Ensaios de Migração de Leucócitos
Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/imunologia
[Mh] Termos MeSH secundário: Antígenos/imunologia
Linfócitos B/imunologia
Citocinas/metabolismo
Eosinófilos/imunologia
Seres Humanos
Imunoglobulina E
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Sensibilidade e Especificidade
Subpopulações de Linfócitos T/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens); 0 (Cytokines); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00174-1


  2 / 106 MEDLINE  
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[PMID]:28424238
[Au] Autor:Gough P; Ganesan S; Datta SK
[Ad] Endereço:Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and.
[Ti] Título:IL-20 Signaling in Activated Human Neutrophils Inhibits Neutrophil Migration and Function.
[So] Source:J Immunol;198(11):4373-4382, 2017 Jun 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neutrophils possess multiple antimicrobial mechanisms that are critical for protection of the host against infection with extracellular microbes, such as the bacterial pathogen Recruitment and activation of neutrophils at sites of infection are driven by cytokine and chemokine signals that directly target neutrophils via specific cell surface receptors. The IL-20 subfamily of cytokines has been reported to act at epithelial sites and contribute to psoriasis, wound healing, and anti-inflammatory effects during infection. However, the ability of these cytokines to directly affect neutrophil function remains incompletely understood. In this article, we show that human neutrophils altered their expression of IL-20R chains upon migration and activation in vivo and in vitro. Such activation of neutrophils under conditions mimicking infection with conferred responsiveness to IL-20 that manifested as modification of actin polymerization and inhibition of a broad range of actin-dependent functions, including phagocytosis, granule exocytosis, and migration. Consistent with the previously described homeostatic and anti-inflammatory properties of IL-20 on epithelial cells, the current study provides evidence that IL-20 directly targets and inhibits key inflammatory functions of neutrophils during infection with .
[Mh] Termos MeSH primário: Interleucinas/metabolismo
Ativação de Neutrófilo
Neutrófilos/imunologia
Neutrófilos/fisiologia
Receptores de Interleucina/imunologia
Transdução de Sinais
Staphylococcus aureus/imunologia
[Mh] Termos MeSH secundário: Brônquios/citologia
Brônquios/microbiologia
Ensaios de Migração de Leucócitos
Movimento Celular
Citocinas/biossíntese
Citocinas/imunologia
Células Epiteliais/imunologia
Células Epiteliais/microbiologia
Exocitose
Seres Humanos
Interleucinas/imunologia
Neutrófilos/metabolismo
Neutrófilos/microbiologia
Fagocitose
Receptores de Interleucina/genética
Receptores de Interleucina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukins); 0 (Receptors, Interleukin); 0 (interleukin 20); 0 (interleukin-20 receptor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700253


  3 / 106 MEDLINE  
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[PMID]:28214870
[Au] Autor:Haruna T; Soga M; Morioka Y; Imura K; Furue Y; Yamamoto M; Hayakawa J; Deguchi M; Arimura A; Yasui K
[Ad] Endereço:Drug Discovery and Disease Research Laboratory,SHIONOGI & Co., Ltd., Osaka, Japan.
[Ti] Título:The Inhibitory Effect of S-777469, a Cannabinoid Type 2 Receptor Agonist, on Skin Inflammation in Mice.
[So] Source:Pharmacology;99(5-6):259-267, 2017.
[Is] ISSN:1423-0313
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:We investigated the effects of S-777469 (1-[[6-Ethyl-1-[4-fluorobenzyl]-5-methyl-2-oxo-1, 2-dihydropyridine-3-carbonyl]amino]-cyclohexanecarboxylic acid), a novel cannabinoid type 2 receptor (CB2) agonist, on 1-fluoro-2,4-dinitrobenzene (DNFB)-induced ear inflammation and mite antigen-induced dermatitis in mice. The oral administration of S-777469 significantly suppressed DNFB-induced ear swelling in a dose-dependent manner. In addition, S-777469 significantly alleviated mite antigen-induced atopic dermatitis-like skin lesions in NC/Nga mice. A histological analysis revealed that S-777469 significantly reduced the epidermal thickness and the number of mast cells infiltrating skin lesions. We demonstrated that S-777469 inhibited mite antigen-induced eosinophil accumulation in skin lesions and an endogenous CB2 ligand, 2-arachidonoylglycerol (2-AG)-induced eosinophil migration in vitro. Moreover, we confirmed that 2-AG levels significantly increased in skin lesions of mite antigen-induced dermatitis model. Together, these results suggest that S-777469 inhibits skin inflammation in mice by blocking the activities of 2-AG.
[Mh] Termos MeSH primário: Inflamação/tratamento farmacológico
Piridonas/farmacologia
Piridonas/uso terapêutico
Receptor CB2 de Canabinoide/agonistas
Pele/efeitos dos fármacos
Pele/patologia
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/antagonistas & inibidores
Ácidos Araquidônicos/metabolismo
Ensaios de Migração de Leucócitos
Dermatite Atópica/tratamento farmacológico
Dermatite Atópica/metabolismo
Dinitrofluorbenzeno
Relação Dose-Resposta a Droga
Endocanabinoides/antagonistas & inibidores
Endocanabinoides/metabolismo
Glicerídeos/antagonistas & inibidores
Glicerídeos/metabolismo
Inflamação/induzido quimicamente
Masculino
Camundongos
Infestações por Ácaros/tratamento farmacológico
Infestações por Ácaros/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Cnr2 protein, mouse); 0 (Endocannabinoids); 0 (Glycerides); 0 (Pyridones); 0 (Receptor, Cannabinoid, CB2); 0 (S-777469); 8D239QDW64 (glyceryl 2-arachidonate); D241E059U6 (Dinitrofluorobenzene)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170220
[St] Status:MEDLINE
[do] DOI:10.1159/000455916


  4 / 106 MEDLINE  
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[PMID]:28167251
[Au] Autor:Havixbeck JJ; Rieger AM; Churchill LJ; Barreda DR
[Ad] Endereço:Department of Biological Sciences, University of Alberta, Edmonton, Canada.
[Ti] Título:Neutrophils exert protection in early Aeromonas veronii infections through the clearance of both bacteria and dying macrophages.
[So] Source:Fish Shellfish Immunol;63:18-30, 2017 Apr.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aeromonas veronii is a gram-negative opportunistic pathogen capable of infecting both fish and mammals. Left untreated, natural infection in fish can prove fatal and result in irreparable damage to the aquaculture industry. Neutrophils are essential innate effector cells that play critical roles in pathogen defense. Our aim was to investigate the immunological roles of teleost neutrophils during infection with A. veronii. We began by examining the functional defenses of neutrophils in vitro, where neutrophils efficiently killed the pathogen. In addition, we developed an in vivo infection model to assess the roles of neutrophils during an infection in goldfish. This allowed us to explore the complex dynamics between immune cells and Aeromonas veronii. Interestingly, our studies found that neutrophils are capable of sensing a diverse range of dead and dying cells, resulting in varying downstream responses. Herein, we report that neutrophils internalized dead or dying macrophages previously infected with A. veronii. Moreover, once internalized, neutrophils went on to display classical pro-inflammatory ROS responses, in contrast to the more typical anti-inflammatory responses seen in cells following the uptake of a dead host cell. This led us to hypothesize that during infection, neutrophils are capable of simultaneously clearing dead and dying cells as well as A. veronii. This study provides additional insights into the complex mechanisms by which neutrophils operate within an inflammatory site and contribute to the induction and regulation of acute inflammatory responses.
[Mh] Termos MeSH primário: Aeromonas veronii/fisiologia
Doenças dos Peixes/imunologia
Carpa Dourada
Infecções por Bactérias Gram-Negativas/veterinária
Inflamação/veterinária
Neutrófilos/imunologia
[Mh] Termos MeSH secundário: Animais
Ensaios de Migração de Leucócitos/veterinária
Doenças dos Peixes/microbiologia
Infecções por Bactérias Gram-Negativas/imunologia
Infecções por Bactérias Gram-Negativas/microbiologia
Inflamação/imunologia
Inflamação/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE


  5 / 106 MEDLINE  
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[PMID]:27693845
[Au] Autor:Tawara S; Sakai T; Matsuzaki O
[Ad] Endereço:Laboratory for Pharmacology, Pharmaceuticals Research Center, Asahi Kasei Pharma Corporation, Shizuoka, Japan. Electronic address: tawara.sc@om.asahi-kasei.co.jp.
[Ti] Título:Anti-inflammatory and anti-fibrinolytic effects of thrombomodulin alfa through carboxypeptidase B2 in the presence of thrombin.
[So] Source:Thromb Res;147:72-79, 2016 Nov.
[Is] ISSN:1879-2472
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Thrombomodulin (TM) alfa, a recombinant human soluble TM, enhances activation of pro-carboxypeptidase B2 (pro-CPB2) by thrombin. Activated pro-CPB2 (CPB2) exerts anti-inflammatory and anti-fibrinolytic activities. Therefore, TM alfa may also have anti-inflammatory and anti-fibrinolytic effects through CPB2. However, these effects of TM alfa have not been elucidated. In the present study, we investigated the effects of TM alfa on inactivation of complement component C5a as an anti-inflammatory effect and prolongation of clot lysis time as an anti-fibrinolytic effect via CPB2 in vitro. METHODS: CPB2 activity and tissue factor-induced thrombin generation was examined by a chromogenic assay. C5a inactivation was evaluated by C-terminal cleavage of C5a and inhibition of C5a-induced human neutrophil migration. Clot lysis time prolongation was examined by a tissue-type plasminogen activator-induced clot lysis assay. RESULTS: CPB2 activity in human plasma was increased by TM alfa and thrombin in a concentration-dependent manner. TM alfa inhibited tissue factor-induced thrombin generation and enhanced pro-CPB2 activation in human plasma simultaneously. The mass spectrum of C5a treated with TM alfa, thrombin, and pro-CPB2 was decreased at 156m/z, indicating that TM alfa enhanced the processing of C5a to C-terminal-cleaved C5a, an inactive form of C5a. C5a-induced human neutrophil migration was decreased after C5a treatment with TM alfa, thrombin, and pro-CPB2. TM alfa prolonged the clot lysis time in human plasma, and this effect was completely abolished by addition of a CPB2 inhibitor. CONCLUSIONS: TM alfa exerts anti-inflammatory and anti-fibrinolytic effects through CPB2 in the presence of thrombin in vitro.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Carboxipeptidase B2/imunologia
Fibrinolíticos/farmacologia
Trombina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Ensaios de Migração de Leucócitos
Inibição de Migração Celular/efeitos dos fármacos
Complemento C5a/imunologia
Ativação Enzimática/efeitos dos fármacos
Tempo de Lise do Coágulo de Fibrina
Seres Humanos
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Proteínas Recombinantes/farmacologia
Trombina/imunologia
Trombomodulina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ART123); 0 (Anti-Inflammatory Agents); 0 (Fibrinolytic Agents); 0 (Recombinant Proteins); 0 (Thrombomodulin); 80295-54-1 (Complement C5a); EC 3.4.17.20 (Carboxypeptidase B2); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE


  6 / 106 MEDLINE  
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[PMID]:27638120
[Au] Autor:Sipka A; Pomeroy B; Klaessig S; Schukken Y
[Ad] Endereço:Quality Milk Production Services, Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA. Electronic address: ass233@cornell.edu.
[Ti] Título:Bovine natural killer cells are present in Escherichia coli infected mammary gland tissue and show antimicrobial activity in vitro.
[So] Source:Comp Immunol Microbiol Infect Dis;48:54-60, 2016 Oct.
[Is] ISSN:1878-1667
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are early responders in bacterial infections but their role in bovine mastitis has not been characterized. For the first time, we show the presence of NK cells (NKp46(+)/CD3(-)) in bovine mammary gland tissue after an intramammary challenge with Escherichia (E.) coli. A small number of NK cells was detected in milk from quarters before and during an E. coli challenge. In vitro cultures of primary bovine mammary gland epithelial cells stimulated with UV irradiated E. coli induced significant migration of peripheral blood NK cells (pbNK) within 2h. Furthermore, pbNK cells significantly reduced counts of live E. coli in vitro within 2h of culture. The results show that bovine NK cells have the capacity to migrate to the site of infection and produce antibacterial mediators. These findings introduce NK cells as a leukocyte population in the mammary gland with potential functions in the innate immune response in bovine mastitis.
[Mh] Termos MeSH primário: Infecções por Escherichia coli/veterinária
Escherichia coli/imunologia
Células Matadoras Naturais/imunologia
Mastite Bovina/imunologia
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Bovinos
Ensaios de Migração de Leucócitos
Células Epiteliais/microbiologia
Escherichia coli/fisiologia
Infecções por Escherichia coli/microbiologia
Feminino
Imunidade Inata
Glândulas Mamárias Animais/imunologia
Glândulas Mamárias Animais/microbiologia
Mastite Bovina/microbiologia
Leite/citologia
Leite/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170123
[Lr] Data última revisão:
170123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160918
[St] Status:MEDLINE


  7 / 106 MEDLINE  
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[PMID]:27536946
[Au] Autor:Zhu XQ; Lu W; Chen Y; Cheng XF; Qiu JY; Xu Y; Sun Y
[Ad] Endereço:Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
[Ti] Título:Effects of Porphyromonas gingivalis LipopolysaccharideTolerized Monocytes on Inflammatory Responses in Neutrophils.
[So] Source:PLoS One;11(8):e0161482, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Periodontitis is a chronic inflammatory disease induced by bacteria. Exposure of the host to periodontal pathogens and their virulence factors induces a state of hyporesponsiveness to subsequent stimulations, which is termed endotoxin tolerance. The role and mechanism of lipopolysaccharide (LPS)-tolerized monocytes in inflammatory responses in neutrophils are currently unclear. Here, conditioned supernatants were collected from THP-1 cells treated with or without repeated 1 µg/ml Porphyromonas gingivalis (P.gingivalis) LPS. The chemotactic response of freshly isolated neutrophils recruited by supernatants was determined by a transwell migration assay, which demonstrated a reduced migration of neutrophils stimulated with supernatants from tolerized THP-1 cells in comparison to non-tolerized THP-1 cells. In addition, there was a marked increase in reactive oxygen species (ROS) generation and a significant decrease in Caspase 3 activities in neutrophils treated with supernatants from THP-1 cells that were treated repeatedly with P.gingivalis LPS in comparison to single treatment. A cytokine antibody array was then used to assess cytokine expression patterns in THP-1 cells. In tolerized THP-1 cells, 43 cytokine (43/170) expression levels were decreased, including chemokine ligand 23 (CCL23) and IFN-γ, while 11 cytokine (11/170) expression levels were increased, such as death receptor 6 (DR6). Furthermore, there was decreased production of IFN-γ and epithelial neutrophil activating peptide-78 (ENA-78) in THP-1 cells after stimulation with repeated P. gingivalis LPS in comparison to single challenge, which was confirmed by ELISA. Therefore, P.gingivalis LPS- tolerized THP-1 cells were able to depress neutrophil chemotaxis and apoptosis, and contribute to respiratory burst, which might be related to the changes in cytokine expression patterns in THP-1 cells.
[Mh] Termos MeSH primário: Inflamação/fisiopatologia
Lipopolissacarídeos/metabolismo
Monócitos/fisiologia
Neutrófilos/fisiologia
Porphyromonas gingivalis/fisiologia
[Mh] Termos MeSH secundário: Apoptose
Linhagem Celular
Ensaios de Migração de Leucócitos
Citocinas/metabolismo
Seres Humanos
Inflamação/microbiologia
Espécies Reativas de Oxigênio/metabolismo
Explosão Respiratória
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Lipopolysaccharides); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0161482


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[PMID]:27035130
[Au] Autor:Joly S; Rhea L; Volk P; Moreland JG; Dunnwald M
[Ad] Endereço:Department of Internal Medicine, The University of Iowa, Iowa City, IA, United States of America.
[Ti] Título:Interferon Regulatory Factor 6 Has a Protective Role in the Host Response to Endotoxic Shock.
[So] Source:PLoS One;11(4):e0152385, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interferon Regulatory Factor (IRF) 6, a member of the IRF family, is essential for epidermal and orofacial embryonic development. Irf6 is strongly expressed in keratinocytes, in which it regulates epidermal proliferation, differentiation, and migration. A recent role for Irf6 in Toll-like receptor 2-dependent chemokine gene expression was also reported in an epithelial cell line. However, a function for Irf6 in innate immune cells was not previously reported. In the present study, we investigated the expression and function of Irf6 in bone marrow-derived neutrophils and macrophages. We show here, using a conditional knockout of Irf6 in lysosymeM expressing cells, that Irf6 is required for resistance to LPS-induced endotoxic shock. In addition, Irf6-deficient bone marrow-derived neutrophils exhibited increased chemotactic index and velocity compared with wild-type cells in vitro. TLR4-specific KC and IL6 secretions were upregulated in Irf6-deficient bone marrow-derived macrophages in vitro. These cells also exhibited an increased level of phosphorylated IkBa. Collectively, our findings suggest a role for Irf6 in the resistance to endotoxic shock due to NFk-B-mediated alteration of cytokine production.
[Mh] Termos MeSH primário: Fatores Reguladores de Interferon/imunologia
Macrófagos/imunologia
Neutrófilos/imunologia
Choque Séptico/imunologia
[Mh] Termos MeSH secundário: Animais
Ensaios de Migração de Leucócitos
Células Cultivadas
Quimiotaxia
Citocinas/imunologia
Feminino
Imunidade Celular
Imunidade Inata
Lipopolissacarídeos/imunologia
Macrófagos/citologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/imunologia
Neutrófilos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cytokines); 0 (IRF6 protein, mouse); 0 (Interferon Regulatory Factors); 0 (Lipopolysaccharides); 0 (NF-kappa B)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170130
[Lr] Data última revisão:
170130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160402
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0152385


  9 / 106 MEDLINE  
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[PMID]:26819316
[Au] Autor:Jones CN; Hoang AN; Martel JM; Dimisko L; Mikkola A; Inoue Y; Kuriyama N; Yamada M; Hamza B; Kaneki M; Warren HS; Brown DE; Irimia D
[Ad] Endereço:BioMEMS Resource Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA;
[Ti] Título:Microfluidic assay for precise measurements of mouse, rat, and human neutrophil chemotaxis in whole-blood droplets.
[So] Source:J Leukoc Biol;100(1):241-7, 2016 Jul.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal models of human disease differ in innate immune responses to stress, pathogens, or injury. Precise neutrophil phenotype measurements could facilitate interspecies comparisons. However, such phenotype comparisons could not be performed accurately with the use of current assays, as they require the separation of neutrophils from blood using species-specific protocols, and they introduce distinct artifacts. Here, we report a microfluidic technology that enables robust characterization of neutrophil migratory phenotypes in a manner independent of the donor species and performed directly in a droplet of whole blood. The assay relies on the particular ability of neutrophils to deform actively during chemotaxis through microscale channels that block the advance of other blood cells. Neutrophil migration is measured directly in blood, in the presence of other blood cells and serum factors. Our measurements reveal important differences among migration counts, velocity, and directionality among neutrophils from 2 common mouse strains, rats, and humans.
[Mh] Termos MeSH primário: Ensaios de Migração de Leucócitos/métodos
Quimiotaxia de Leucócito/fisiologia
Técnicas Analíticas Microfluídicas/instrumentação
Técnicas Analíticas Microfluídicas/métodos
Neutrófilos/citologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160129
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.5TA0715-310RR


  10 / 106 MEDLINE  
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[PMID]:26779602
[Au] Autor:Minnich M; Tagoh H; Bönelt P; Axelsson E; Fischer M; Cebolla B; Tarakhovsky A; Nutt SL; Jaritz M; Busslinger M
[Ad] Endereço:Research Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria.
[Ti] Título:Multifunctional role of the transcription factor Blimp-1 in coordinating plasma cell differentiation.
[So] Source:Nat Immunol;17(3):331-43, 2016 Mar.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor Blimp-1 is necessary for the generation of plasma cells. Here we studied its functions in plasmablast differentiation by identifying regulated Blimp-1 target genes. Blimp-1 promoted the migration and adhesion of plasmablasts. It directly repressed genes encoding several transcription factors and Aicda (which encodes the cytidine deaminase AID) and thus silenced B cell-specific gene expression, antigen presentation and class-switch recombination in plasmablasts. It directly activated genes, which led to increased expression of the plasma cell regulator IRF4 and proteins involved in immunoglobulin secretion. Blimp-1 induced the transcription of immunoglobulin genes by controlling the 3' enhancers of the loci encoding the immunoglobulin heavy chain (Igh) and κ-light chain (Igk) and, furthermore, regulated the post-transcriptional expression switch from the membrane-bound form of the immunoglobulin heavy chain to its secreted form by activating Ell2 (which encodes the transcription-elongation factor ELL2). Notably, Blimp-1 recruited chromatin-remodeling and histone-modifying complexes to regulate its target genes. Hence, many essential functions of plasma cells are under the control of Blimp-1.
[Mh] Termos MeSH primário: Diferenciação Celular/imunologia
Cadeias Pesadas de Imunoglobulinas/imunologia
Cadeias kappa de Imunoglobulina/imunologia
Fatores Reguladores de Interferon/imunologia
Plasmócitos/imunologia
Fatores de Transcrição/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Linfócitos B/metabolismo
Adesão Celular/genética
Adesão Celular/imunologia
Diferenciação Celular/genética
Ensaios de Migração de Leucócitos
Movimento Celular/genética
Movimento Celular/imunologia
Imunoprecipitação da Cromatina
Ensaio de Desvio de Mobilidade Eletroforética
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Regulação da Expressão Gênica
Células HEK293
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Cadeias Pesadas de Imunoglobulinas/genética
Cadeias kappa de Imunoglobulina/genética
Fatores Reguladores de Interferon/genética
Espectrometria de Massas
Camundongos
Plasmócitos/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Análise de Sequência de DNA
Análise de Sequência de RNA
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin kappa-Chains); 0 (Interferon Regulatory Factors); 0 (Prdm1 protein, mouse); 0 (Transcription Factors); 0 (interferon regulatory factor-4); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3349



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