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[PMID]:29277802
[Au] Autor:Pelissier A; Franke O; Darai E; Houvenaeghel G; Chereau E; Rouzier R
[Ad] Endereço:Department of Oncologic Surgery, Centre René Huguenin, Institut Curie, Saint Cloud, France a.komorek@gmail.com.
[Ti] Título:Value of Diaphragmatic Surgery During Interval Debulking Surgery.
[So] Source:Anticancer Res;38(1):411-416, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The aim of this study was to assess the value of diaphragmatic surgery to achieve optimal debulking in patients with advanced ovarian cancer treated by neoadjuvant chemotherapy (NAC). PATIENTS AND METHODS: This is a retrospective review of the medical records of 182 patients. Diaphragmatic surgery was performed during interval debulking surgery (IDS) in 74 patients between January 2002 and December 2014. The patients were divided in 2 groups: with or without histological residual diaphragmatic disease. The time-course of serum CA125 levels, cytoreductive outcome, overall survival (OS) and relapse-free survival (RFS) were analyzed. Patients without diaphragmatic peritonectomy (DP) during IDS were included in the survival analysis. RESULTS: One hundred thirty-two (72.5%) patients had FIGO stage III disease and 43 (23.6%) patients had stage IV disease. Histological examination of DP was positive in 45 patients and negative in 29 patients. CA125 normalization after the 3rd cycle of NAC was significantly associated with negative DP. OS tended to be higher in the DP-negative group (37.8 months vs 19 months, p=0.1). Median OS was 40.7 months in the case of IDS without DP and 22 months in the case of IDS with DP (p=0.048). CONCLUSION: Evaluation of residual diaphragmatic disease can be difficult after NAC. The CA125 tumor marker appears to be a useful tool to define the indications for DP. Diaphragmatic surgery after NAC may be of limited value.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Procedimentos Cirúrgicos de Citorredução/métodos
Diafragma/cirurgia
Subunidade alfa de Receptor de Interleucina-5/sangue
Neoplasias Ovarianas/cirurgia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Intervalo Livre de Doença
Feminino
Seres Humanos
Meia-Idade
Terapia Neoadjuvante
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/patologia
Estudos Retrospectivos
Análise de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Interleukin-5 Receptor alpha Subunit)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:28737051
[Au] Autor:Matera MG; Calzetta L; Rinaldi B; Cazzola M
[Ad] Endereço:a Department of Experimental Medicine , University of Campania Luigi Vanvitelli , Naples , Italy.
[Ti] Título:Pharmacokinetic/pharmacodynamic drug evaluation of benralizumab for the treatment of asthma.
[So] Source:Expert Opin Drug Metab Toxicol;13(9):1007-1013, 2017 Sep.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: In many severe asthmatics, eosinophils cause inflammation and airways hyperresponsiveness, resulting in frequent exacerbations, impaired lung function, and reduced quality of life. Interleukin-5 (IL-5) is a key cytokine for eosinophil growth, differentiation, recruitment, activation, and survival. Anti-IL-5-based therapies (mepolizumab and reslizumab are humanized monoclonal antibodies (hmAbs) that recognize free IL-5, benralizumab is a hmAb directed at the α subunit of the IL-5R) target the IL-5-signaling in eosinophilic asthma. Areas covered: The pharmacodynamic/pharmacokinetic profile of benralizumab and how it provided indications that permitted optimization of the design and timelines of the pivotal trials are described. Expert opinion: Benralizumab has the advantage over other anti-IL-5 therapies to target the IL-5Rα itself. Afucosylation enhances its interaction with its binding site and facilitates its pharmacological activity. Other benefits of benralizumab are fast (within 24 h) depletion of peripheral blood eosinophils, potent suppressive activity of bone marrow eosinophils and eosinophil precursors, tissue eosinophil apoptosis regardless of the presence of eosinophil survival factors and even at low IL-5R densities. The fact that benralizumab is dosed subcutaneously and is equally effective when given every eight weeks instead than every four weeks provides patients with convenience of self-administration and make it appealing for patients who dislike injections.
[Mh] Termos MeSH primário: Antiasmáticos/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Asma/tratamento farmacológico
[Mh] Termos MeSH secundário: Antiasmáticos/farmacologia
Anticorpos Monoclonais Humanizados/farmacologia
Asma/imunologia
Asma/patologia
Eosinófilos/metabolismo
Seres Humanos
Interleucina-5/antagonistas & inibidores
Subunidade alfa de Receptor de Interleucina-5/antagonistas & inibidores
Qualidade de Vida
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Antibodies, Monoclonal, Humanized); 0 (Interleukin-5); 0 (Interleukin-5 Receptor alpha Subunit); 71492GE1FX (benralizumab)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2017.1359253


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[PMID]:28574721
[Au] Autor:Forno E; Wang T; Yan Q; Brehm J; Acosta-Perez E; Colon-Semidey A; Alvarez M; Boutaoui N; Cloutier MM; Alcorn JF; Canino G; Chen W; Celedón JC
[Ad] Endereço:1 Division of Pediatric Pulmonary Medicine, Allergy, and Immunology, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, Pennsylvania.
[Ti] Título:A Multiomics Approach to Identify Genes Associated with Childhood Asthma Risk and Morbidity.
[So] Source:Am J Respir Cell Mol Biol;57(4):439-447, 2017 Oct.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Childhood asthma is a complex disease. In this study, we aim to identify genes associated with childhood asthma through a multiomics "vertical" approach that integrates multiple analytical steps using linear and logistic regression models. In a case-control study of childhood asthma in Puerto Ricans (n = 1,127), we used adjusted linear or logistic regression models to evaluate associations between several analytical steps of omics data, including genome-wide (GW) genotype data, GW methylation, GW expression profiling, cytokine levels, asthma-intermediate phenotypes, and asthma status. At each point, only the top genes/single-nucleotide polymorphisms/probes/cytokines were carried forward for subsequent analysis. In step 1, asthma modified the gene expression-protein level association for 1,645 genes; pathway analysis showed an enrichment of these genes in the cytokine signaling system (n = 269 genes). In steps 2-3, expression levels of 40 genes were associated with intermediate phenotypes (asthma onset age, forced expiratory volume in 1 second, exacerbations, eosinophil counts, and skin test reactivity); of those, methylation of seven genes was also associated with asthma. Of these seven candidate genes, IL5RA was also significant in analytical steps 4-8. We then measured plasma IL-5 receptor α levels, which were associated with asthma age of onset and moderate-severe exacerbations. In addition, in silico database analysis showed that several of our identified IL5RA single-nucleotide polymorphisms are associated with transcription factors related to asthma and atopy. This approach integrates several analytical steps and is able to identify biologically relevant asthma-related genes, such as IL5RA. It differs from other methods that rely on complex statistical models with various assumptions.
[Mh] Termos MeSH primário: Asma
Regulação da Expressão Gênica
Genômica
Subunidade alfa de Receptor de Interleucina-5
Modelos Biológicos
Polimorfismo Genético
[Mh] Termos MeSH secundário: Adolescente
Asma/genética
Asma/metabolismo
Asma/mortalidade
Estudos de Casos e Controles
Criança
Pré-Escolar
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Subunidade alfa de Receptor de Interleucina-5/biossíntese
Subunidade alfa de Receptor de Interleucina-5/genética
Masculino
Porto Rico/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (IL5RA protein, human); 0 (Interleukin-5 Receptor alpha Subunit)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0002OC


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[PMID]:28530840
[Au] Autor:Nair P; Wenzel S; Rabe KF; Bourdin A; Lugogo NL; Kuna P; Barker P; Sproule S; Ponnarambil S; Goldman M; ZONDA Trial Investigators
[Ad] Endereço:From McMaster University and St. Joseph's Healthcare, Hamilton, ON, Canada (P.N.); University of Pittsburgh, Pittsburgh (S.W.); LungenClinic Grosshansdorf and Department of Medicine, Airway Research Center North of the German Center for Lung Research, Christian Albrechts University, Kiel, Germany (K
[Ti] Título:Oral Glucocorticoid-Sparing Effect of Benralizumab in Severe Asthma.
[So] Source:N Engl J Med;376(25):2448-2458, 2017 06 22.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Many patients with severe asthma rely on oral glucocorticoids to manage their disease. We investigated whether benralizumab, a monoclonal antibody directed against the alpha subunit of the interleukin-5 receptor that significantly reduces the incidence of asthma exacerbations, was also effective as an oral glucocorticoid-sparing therapy in patients relying on oral glucocorticoids to manage severe asthma associated with eosinophilia. METHODS: In a 28-week randomized, controlled trial, we assessed the effects of benralizumab (at a dose of 30 mg administered subcutaneously either every 4 weeks or every 8 weeks [with the first three doses administered every 4 weeks]) versus placebo on the reduction in the oral glucocorticoid dose while asthma control was maintained in adult patients with severe asthma. The primary end point was the percentage change in the oral glucocorticoid dose from baseline to week 28. Annual asthma exacerbation rates, lung function, symptoms, and safety were assessed. RESULTS: Of 369 patients enrolled, 220 underwent randomization and started receiving benralizumab or placebo. The two benralizumab dosing regimens significantly reduced the median final oral glucocorticoid doses from baseline by 75%, as compared with a reduction of 25% in the oral glucocorticoid doses in the placebo group (P<0.001 for both comparisons). The odds of a reduction in the oral glucocorticoid dose were more than 4 times as high with benralizumab as with placebo. Among the secondary outcomes, benralizumab administered every 4 weeks resulted in an annual exacerbation rate that was 55% lower than the rate with placebo (marginal rate, 0.83 vs. 1.83, P=0.003), and benralizumab administered every 8 weeks resulted in an annual exacerbation rate that was 70% lower than the rate with placebo (marginal rate, 0.54 vs. 1.83, P<0.001). At 28 weeks, there was no significant effect of either benralizumab regimen on the forced expiratory volume in 1 second (FEV ), as compared with placebo. The effects on various measures of asthma symptoms were mixed, with some showing significant changes in favor of benralizumab and others not showing significant changes. Frequencies of adverse events were similar between each benralizumab group and the placebo group. CONCLUSIONS: Benralizumab showed significant, clinically relevant benefits, as compared with placebo, on oral glucocorticoid use and exacerbation rates. These effects occurred without a sustained effect on the FEV . (Funded by AstraZeneca; ZONDA ClinicalTrials.gov number, NCT02075255 .).
[Mh] Termos MeSH primário: Antiasmáticos/uso terapêutico
Anticorpos Monoclonais Humanizados/uso terapêutico
Asma/tratamento farmacológico
Glucocorticoides/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Adulto
Antiasmáticos/administração & dosagem
Antiasmáticos/efeitos adversos
Anticorpos Monoclonais Humanizados/efeitos adversos
Relação Dose-Resposta a Droga
Método Duplo-Cego
Feminino
Seres Humanos
Injeções Subcutâneas
Subunidade alfa de Receptor de Interleucina-5/antagonistas & inibidores
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Antibodies, Monoclonal, Humanized); 0 (Glucocorticoids); 0 (IL5RA protein, human); 0 (Interleukin-5 Receptor alpha Subunit); 71492GE1FX (benralizumab)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170523
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1703501


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[PMID]:28132394
[Au] Autor:Zhou Y; Li C; Li D; Zheng Y; Wang J
[Ad] Endereço:Department of Basic Medicine, Luohe Medical College, Luohe, 462002, China.
[Ti] Título:IL-5 blocks apoptosis and tau hyperphosphorylation induced by Aß peptide in PC12 cells.
[So] Source:J Physiol Biochem;73(2):259-266, 2017 May.
[Is] ISSN:1877-8755
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:The primary features of Alzheimer's disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid ß (Aß) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aß -induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aß -evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/metabolismo
Apoptose
Subunidade alfa de Receptor de Interleucina-5/agonistas
Interleucina-5/metabolismo
Neurônios/metabolismo
Fragmentos de Peptídeos/metabolismo
Processamento de Proteína Pós-Traducional
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Animais
Apoptose/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Ativação Enzimática/efeitos dos fármacos
Subunidade alfa de Receptor de Interleucina-5/antagonistas & inibidores
Subunidade alfa de Receptor de Interleucina-5/genética
Subunidade alfa de Receptor de Interleucina-5/metabolismo
Janus Quinase 2/antagonistas & inibidores
Janus Quinase 2/química
Janus Quinase 2/metabolismo
Proteínas do Tecido Nervoso/agonistas
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/patologia
Células PC12
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Pirrolidinas/farmacologia
Interferência de RNA
Ratos
Transdução de Sinais/efeitos dos fármacos
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Interleukin-5); 0 (Interleukin-5 Receptor alpha Subunit); 0 (Mapt protein, rat); 0 (Nerve Tissue Proteins); 0 (Peptide Fragments); 0 (Protein Kinase Inhibitors); 0 (Pyrrolidines); 0 (Sulfonamides); 0 (TG101348); 0 (amyloid beta-protein (25-35)); 0 (tau Proteins); EC 2.7.10.2 (Jak2 protein, rat); EC 2.7.10.2 (Janus Kinase 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE
[do] DOI:10.1007/s13105-017-0550-8


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[PMID]:27992791
[Au] Autor:Chen Y; Zhang Y; Xu M; Luan J; Piao S; Chi S; Wang H
[Ad] Endereço:The Second Department of Paediatrics, the First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, People's Republic of China.
[Ti] Título:Catalpol alleviates ovalbumin-induced asthma in mice: Reduced eosinophil infiltration in the lung.
[So] Source:Int Immunopharmacol;43:140-146, 2017 Feb.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Radix Rehmanniae Preparata is a traditional Chinese herbal medicine used to treat asthma, and catalpol is one of the main active ingredients in this herb. In the present study, the effects of catalpol on asthma and the underlying mechanism were explored. METHODS: Mice with ovalbumin (OVA)-induced asthma were given 5 or 10mg/kg catalpol from Day 15 to Day 28 (intraperitoneal injection). Histopathologic changes were detected by Hematoxylin and Eosin staining and Periodic Acid Schiff staining. The levels of IgE, interleukin (IL)-4, IL-5 and eotaxin were measured by ELISA. The numbers of lymphocytes, monocytes, basophils and eosinophils in the bronchoalveolar lavage fluid were determined by Wright-Giemsa staining. The expression and distribution of eotaxin and C-C chemokine receptor 3 (CCR3) were detected by immunohistochemistry and immunofluorescence. The expression of interleukin-5 receptor α (IL-5Rα) was detected by Western blot assay. RESULTS: Catalpol inhibited OVA-induced inflammation and IgE secretion in the lung. OVA-induced type 2 inflammation was suppressed by catalpol as evidenced by decreased levels of IL-4 and IL-5. Moreover, catalpol inhibited the aberrant eosinophil infiltration in the lungs, and also suppressed OVA-induced elevation of eosinophil chemokine eotaxin and its receptor CCR3. In addition, IL-5Rα expression in the bone marrow cells derived from catalpol-treated asthmatic mice was lower than that from the untreated asthmatic mice. CONCLUSION: Our study demonstrated that catalpol attenuated OVA-induced asthma and inhibit the infiltration of inflammatory cells, especially eosinophils, into the lung. This study suggests that catalpol may become a promising drug for the treatment of asthma.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Asma/tratamento farmacológico
Medicamentos de Ervas Chinesas/uso terapêutico
Eosinófilos/efeitos dos fármacos
Glucosídeos Iridoides/uso terapêutico
Pulmão/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Movimento Celular/efeitos dos fármacos
Quimiocina CCL11/metabolismo
Eosinófilos/imunologia
Seres Humanos
Imunoglobulina E/metabolismo
Interleucina-4/metabolismo
Interleucina-5/metabolismo
Subunidade alfa de Receptor de Interleucina-5/metabolismo
Pulmão/metabolismo
Pulmão/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Receptores CCR3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Ccl11 protein, mouse); 0 (Ccr3 protein, mouse); 0 (Chemokine CCL11); 0 (Drugs, Chinese Herbal); 0 (Interleukin-5); 0 (Interleukin-5 Receptor alpha Subunit); 0 (Iridoid Glucosides); 0 (Receptors, CCR3); 0 (interleukin-5- receptor alpha, mouse); 207137-56-2 (Interleukin-4); 2415-24-9 (catalpol); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170411
[Lr] Data última revisão:
170411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161220
[St] Status:MEDLINE


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[PMID]:27683753
[Au] Autor:Johnston LK; Hsu CL; Krier-Burris RA; Chhiba KD; Chien KB; McKenzie A; Berdnikovs S; Bryce PJ
[Ad] Endereço:Division of Allergy-Immunology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60610; and.
[Ti] Título:IL-33 Precedes IL-5 in Regulating Eosinophil Commitment and Is Required for Eosinophil Homeostasis.
[So] Source:J Immunol;197(9):3445-3453, 2016 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eosinophils are important in the pathogenesis of many diseases, including asthma, eosinophilic esophagitis, and eczema. Whereas IL-5 is crucial for supporting mature eosinophils (EoMs), the signals that support earlier eosinophil lineage events are less defined. The IL-33R, ST2, is expressed on several inflammatory cells, including eosinophils, and is best characterized for its role during the initiation of allergic responses in peripheral tissues. Recently, ST2 expression was described on hematopoietic progenitor subsets, where its function remains controversial. Our findings demonstrate that IL-33 is required for basal eosinophil homeostasis, because both IL-33- and ST2-deficient mice exhibited diminished peripheral blood eosinophil numbers at baseline. Exogenous IL-33 administration increased EoMs in both the bone marrow and the periphery in wild-type and IL-33-deficient, but not ST2-deficient, mice. Systemic IL-5 was also increased under this treatment, and blocking IL-5 with a neutralizing Ab ablated the IL-33-induced EoM expansion. The homeostatic hypereosinophilia seen in IL-5-transgenic mice was significantly lower with ST2 deficiency despite similar elevations in systemic IL-5. Finally, in vitro treatment of bone marrow cells with IL-33, but not IL-5, led to specific early expansion of IL-5Rα-expressing precursor cells. In summary, our findings establish a basal defect in eosinophilopoiesis in IL-33- and ST2-deficient mice and a mechanism whereby IL-33 supports EoMs by driving both systemic IL-5 production and the expansion of IL-5Rα-expressing precursor cells.
[Mh] Termos MeSH primário: Eosinófilos/fisiologia
Proteína 1 Semelhante a Receptor de Interleucina-1/metabolismo
Interleucina-33/metabolismo
Interleucina-5/metabolismo
Neutrófilos/fisiologia
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/fisiologia
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Regulação da Expressão Gênica
Hematopoese
Homeostase
Seres Humanos
Proteína 1 Semelhante a Receptor de Interleucina-1/genética
Interleucina-33/genética
Interleucina-5/genética
Subunidade alfa de Receptor de Interleucina-5/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Il1rl1 protein, mouse); 0 (Interleukin-1 Receptor-Like 1 Protein); 0 (Interleukin-33); 0 (Interleukin-5); 0 (Interleukin-5 Receptor alpha Subunit); 0 (interleukin-5- receptor alpha, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160930
[St] Status:MEDLINE


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[PMID]:26276876
[Au] Autor:Esnault S; Kelly EA; Shen ZJ; Johansson MW; Malter JS; Jarjour NN
[Ad] Endereço:Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792; sesnault@medicine.wisc.edu.
[Ti] Título:IL-3 Maintains Activation of the p90S6K/RPS6 Pathway and Increases Translation in Human Eosinophils.
[So] Source:J Immunol;195(6):2529-39, 2015 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-5 is a major therapeutic target to reduce eosinophilia. However, all of the eosinophil-activating cytokines, such as IL-5, IL-3, and GM-CSF, are typically present in atopic diseases, including allergic asthma. As a result of the functional redundancy of these three cytokines on eosinophils and the loss of IL-5R on airway eosinophils, it is important to take IL-3 and GM-CSF into account to efficiently reduce tissue eosinophil functions. Moreover, these three cytokines signal through a common ß-chain receptor but yet differentially affect protein production in eosinophils. Notably, the increased ability of IL-3 to induce the production of proteins, such as semaphorin-7A, without affecting mRNA levels suggests a unique influence of IL-3 on translation. The purpose of this study was to identify the mechanisms by which IL-3 distinctively affects eosinophil function compared with IL-5 and GM-CSF, with a focus on protein translation. Peripheral blood eosinophils were used to study intracellular signaling and protein translation in cells activated with IL-3, GM-CSF, or IL-5. We establish that, unlike GM-CSF or IL-5, IL-3 triggers prolonged signaling through activation of ribosomal protein S6 (RPS6) and the upstream kinase 90-kDa ribosomal S6 kinase (p90S6K). Blockade of p90S6K activation inhibited phosphorylation of RPS6 and IL-3-enhanced semaphorin-7A translation. Furthermore, in an allergen-challenged environment, in vivo phosphorylation of RPS6 and p90S6K was enhanced in human airway compared with circulating eosinophils. Our findings provide new insights into the mechanisms underlying differential activation of eosinophils by IL-3, GM-CSF, and IL-5. These observations identify IL-3 and its downstream intracellular signals as novel targets that should be considered to modulate eosinophil functions.
[Mh] Termos MeSH primário: Eosinófilos/fisiologia
Interleucina-3/imunologia
Proteínas Quinases S6 Ribossômicas/metabolismo
Proteína S6 Ribossômica/metabolismo
[Mh] Termos MeSH secundário: Asma/imunologia
Células Cultivadas
Ativação Enzimática
Eosinofilia/imunologia
Eosinófilos/citologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/imunologia
Seres Humanos
Hipersensibilidade/imunologia
Interleucina-5/imunologia
Subunidade alfa de Receptor de Interleucina-5/metabolismo
Fosforilação
RNA Mensageiro/biossíntese
Proteína S6 Ribossômica/genética
Proteínas Quinases S6 Ribossômicas/antagonistas & inibidores
Semaforinas/biossíntese
Semaforinas/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (IL3 protein, human); 0 (IL5 protein, human); 0 (IL5RA protein, human); 0 (Interleukin-3); 0 (Interleukin-5); 0 (Interleukin-5 Receptor alpha Subunit); 0 (RNA, Messenger); 0 (Ribosomal Protein S6); 0 (Semaphorins); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 2.7.11.1 (Ribosomal Protein S6 Kinases)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150816
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1500871


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[PMID]:25704963
[Au] Autor:Mortuaire G; Gengler I; Vandenhende-Szymanski C; Delbeke M; Gatault S; Chevalier D; Prin L; Capron M
[Ad] Endereço:INSERM U995, Université de Lille, Lille, France; EA 2686, Université de Lille, Lille, France; Department of Otorhinolaryngology-Head and Neck Surgery, University Hospital, Lille, France; French Eosinophil Network, University Hospital, Lille, France. Electronic address: g-mortuaire@chru-lille.fr.
[Ti] Título:Immune profile modulation of blood and mucosal eosinophils in nasal polyposis with concomitant asthma.
[So] Source:Ann Allergy Asthma Immunol;114(4):299-307.e2, 2015 Apr.
[Is] ISSN:1534-4436
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is frequently associated with asthma. Mucosal eosinophil (EO) infiltrate has been found to correlate with asthma and disease severity but not necessarily in every patient. Other multifactorial immune processes are required to determine disease endotypes and response to treatment. OBJECTIVE: To evaluate EO immunomodulation for migration and survival in accordance with inflammatory protein profiles and asthmatic status in CRSwNP. METHODS: Ninety-three patients (47 with asthma) with CRSwNP were included. Each patient was staged clinically according to symptom severity and polyp size. Nasal secretions were collected to establish a cytokine profile. The EOs were purified from blood samples and nasal polyps to delineate specific immunophenotypes by flow cytometry and determine in vitro EO survival in relation to asthmatic status. RESULTS: The CRSwNP in patients with asthma was characterized by eosinophilia and a high level of interleukin (IL)-5 in nasal secretions. Although EOs exhibited activation profiles after mucosal migration, there was relative down-expression of IL-5 receptor-α (IL-5Rα) on nasal EOs in patients with asthma. The EO culture with IL-5 and IL-9 showed an antiapoptotic effect in patients with asthma through IL-5Rα modulation. CONCLUSION: Mucosal eosinophilia seems to be induced by EO nasal trapping through modulation of adhesion receptors. In patients with asthma, EO involvement is enhanced by the antiapoptotic synergistic action of T-helper cell type 2 cytokines on IL-5Rα expression. This study shows for the first time that IL-9 is involved in EO homeostasis in CRSwNP and could explain the low benefit of anti-IL-5 therapy for some patients with asthma and nasal polyposis.
[Mh] Termos MeSH primário: Asma/imunologia
Eosinófilos/imunologia
Pólipos Nasais/imunologia
Rinite/imunologia
Sinusite/imunologia
[Mh] Termos MeSH secundário: Asma/complicações
Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/metabolismo
Células Cultivadas
Doença Crônica
Progressão da Doença
Regulação para Baixo
Feminino
Seres Humanos
Interleucina-5/metabolismo
Subunidade alfa de Receptor de Interleucina-5/metabolismo
Interleucina-9/metabolismo
Masculino
Meia-Idade
Pólipos Nasais/complicações
Rinite/complicações
Sinusite/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (IL5RA protein, human); 0 (Interleukin-5); 0 (Interleukin-5 Receptor alpha Subunit); 0 (Interleukin-9)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150406
[Lr] Data última revisão:
150406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150224
[St] Status:MEDLINE


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[PMID]:25523412
[Au] Autor:Miyake Y; Tanaka K; Arakawa M
[Ad] Endereço:Department of Public Health, Ehime University Graduate School of Medicine, Ehime, Japan.
[Ti] Título:IL5RA polymorphisms, smoking and eczema in Japanese women: the Kyushu Okinawa Maternal and Child Health Study.
[So] Source:Int J Immunogenet;42(1):52-7, 2015 Feb.
[Is] ISSN:1744-313X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The present case-control study examined the relationship between IL5RA SNPs and eczema in young adult Japanese women. Cases and control subjects were selected from pregnant women who participated in the baseline survey of the Kyushu Okinawa Maternal and Child Health Study, which is an ongoing prebirth cohort study. Cases comprised 188 women with eczema in the previous 12 months as defined according to the criteria of the International Study of Asthma and Allergies in Childhood (ISAAC), regardless of the presence of a doctor's diagnosis of atopic eczema. Control subjects comprised 1130 women without eczema as defined according to the ISAAC criteria who also had not been diagnosed with atopic eczema by a doctor. Compared with the AA genotype of IL5RA SNP rs17881144, the AT genotype, but not the TT genotype, was significantly associated with a decreased risk of eczema. The ATTAGA haplotype and the GTAGCA haplotype of rs17882210, rs3804797, rs334809, rs9831572, rs6771148 and rs17881144 were significantly associated with an increased risk of eczema. In contrast, the GCTGCA haplotype was significantly related to a decreased risk of eczema. Multiplicative interactions between IL5RA SNPs rs334809 and rs17881144 and smoking with respect to eczema were marginally significant (P = 0.07 and 0.07, respectively). This is the first study to show significant associations between IL5RA SNP rs17881144, the ATTAGA haplotype, the GTAGCA haplotype, and the GCTGCA haplotype and eczema. Smoking may modify the relationships between SNPs rs334809 and rs17881144 and eczema.
[Mh] Termos MeSH primário: Eczema/genética
Haplótipos/genética
Subunidade alfa de Receptor de Interleucina-5/genética
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Feminino
Predisposição Genética para Doença
Seres Humanos
Japão
Polimorfismo de Nucleotídeo Único/genética
Gravidez
Estudos Prospectivos
Fumar/efeitos adversos
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL5RA protein, human); 0 (Interleukin-5 Receptor alpha Subunit)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141220
[St] Status:MEDLINE
[do] DOI:10.1111/iji.12172



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