Base de dados : MEDLINE
Pesquisa : D23.125.320 [Categoria DeCS]
Referências encontradas : 548 [refinar]
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[PMID]:23742077
[Au] Autor:Ueki S; Nishikawa J; Yamauchi Y; Konno Y; Tamaki M; Itoga M; Kobayashi Y; Takeda M; Moritoki Y; Ito W; Chihara J
[Ad] Endereço:Department of Infection, Allergy, Clinical Immunology and Laboratory Medicine, Akita University Graduate School of Medicine, Akita, Japan. ueki-shige@nifty.com
[Ti] Título:Retinoic acids up-regulate functional eosinophil-driving receptor CCR3.
[So] Source:Allergy;68(7):953-6, 2013 Jul.
[Is] ISSN:1398-9995
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Eotaxins and their receptor CCR3 have a definitive role for tissue accumulation of eosinophils both under homeostatic and pathologic conditions. However, physiological stimuli that can up-regulate CCR3 in blood-derived human eosinophils have not been recognized. As a prior gene microarray study revealed up-regulation of CCR3 in eosinophils stimulated with retinoic acids (RAs), the expression of functional CCR3 was examined. We found that 9-cis RA and all-trans RA (ATRA) significantly induced surface CCR3 expression regardless of the presence of IL-3 or IL-5. Pharmacological manipulations with receptor-specific agonists and antagonists indicated that retinoic acid receptor-α activation is critical for CCR3 up-regulation. RA-induced CCR3 was associated with its functional capacity, in terms of the calcium mobilization and chemotactic response to eotaxin-1 (CCL11). Our study suggests an important role of vitamin A derivatives in the tissue accumulation of eosinophils.
[Mh] Termos MeSH primário: Quimiotaxia de Leucócito/efeitos dos fármacos
Dermatite Atópica/sangue
Eosinófilos/efeitos dos fármacos
Receptores CCR3/genética
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Células Cultivadas
Quimiocina CCL24/genética
Quimiocina CCL24/metabolismo
Fatores Quimiotáticos de Eosinófilos/genética
Fatores Quimiotáticos de Eosinófilos/metabolismo
Quimiotaxia de Leucócito/genética
Dermatite Atópica/genética
Eosinófilos/imunologia
Regulação da Expressão Gênica
Seres Humanos
Receptores CCR3/metabolismo
Sensibilidade e Especificidade
Transdução de Sinais/genética
Transdução de Sinais/imunologia
Regulação para Cima
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCR3 protein, human); 0 (Chemokine CCL24); 0 (Chemotactic Factors, Eosinophil); 0 (Receptors, CCR3); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1311
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130608
[St] Status:MEDLINE
[do] DOI:10.1111/all.12175


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[PMID]:21985360
[Au] Autor:Günther C; Wozel G; Meurer M; Pfeiffer C
[Ad] Endereço:University Hospital for Dermatology, Technical University Dresden, Dresden, Germany. claudia.guenther@uniklinikum-dresden.de
[Ti] Título:Up-regulation of CCL11 and CCL26 is associated with activated eosinophils in bullous pemphigoid.
[So] Source:Clin Exp Immunol;166(2):145-53, 2011 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Eosinophils contribute to the pathogenesis of bullous pemphigoid (BP) by secretion of proinflammatory cytokines and proteases. Trafficking of eosinophils into tissue in animal models and asthma depends on interleukin-5 and a family of chemokines named eotaxins, comprising CCL11, CCL24 and CCL26. Up-regulation of CCL11 has been described in BP, but the expression of the other two members of the eotaxin-family, CCL24 and CCL26, has not been investigated. In addition to these chemokines, expression of adhesion molecules associated with eosinophil migration to the skin should be analysed. We demonstrate that similar to CCL11, the concentration of CCL26 was up-regulated in serum and blister fluid of BP patients. In contrast, the concentration of CCL24 was not elevated in sera and blister fluid of the same BP patients. In lesional skin, CCL11 and CCL26 were detected in epidermis and dermis by immunohistochemistry. In contrast to CCL11, CCL26 was expressed strongly by endothelial cells. In line with these findings, eosinophils represented the dominating cell population in BP lesional skin outnumbering other leucocytes. The percentage of eosinophils expressing very late antigen (VLA): VLA-4 (CD49d) and CD11c correlated with their quantity in tissue. Macrophage antigen (MAC)-1 (CD11b/CD18) was expressed constitutively by tissue eosinophils. In conclusion, these data link the up-regulation of the eosinophil chemotactic factor CCL26 in BP to the lesional accumulation of activated eosinophils in the skin. Thereby they broaden the understanding of BP pathogenesis and might indicate new options for therapeutic intervention.
[Mh] Termos MeSH primário: Quimiocina CCL11/sangue
Quimiocinas CC/sangue
Eosinófilos/imunologia
Penfigoide Bolhoso/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Vesícula/imunologia
Antígeno CD11c/biossíntese
Antígenos CD18/biossíntese
Quimiocina CCL24/sangue
Quimiocina CCL26
Fatores Quimiotáticos de Eosinófilos/biossíntese
Fatores Quimiotáticos de Eosinófilos/imunologia
Fatores Quimiotáticos de Eosinófilos/metabolismo
Células Endoteliais/citologia
Células Endoteliais/secreção
Eosinófilos/metabolismo
Eosinófilos/patologia
Feminino
Seres Humanos
Integrina alfa4beta1/biossíntese
Ativação Linfocitária
Antígeno de Macrófago 1/biossíntese
Masculino
Meia-Idade
Penfigoide Bolhoso/patologia
Pele/citologia
Pele/patologia
Pele/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCL11 protein, human); 0 (CCL24 protein, human); 0 (CCL26 protein, human); 0 (CD11c Antigen); 0 (CD18 Antigens); 0 (Chemokine CCL11); 0 (Chemokine CCL24); 0 (Chemokine CCL26); 0 (Chemokines, CC); 0 (Chemotactic Factors, Eosinophil); 0 (Integrin alpha4beta1); 0 (Macrophage-1 Antigen)
[Em] Mês de entrada:1111
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111012
[St] Status:MEDLINE
[do] DOI:10.1111/j.1365-2249.2011.04464.x


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[PMID]:21686182
[Au] Autor:Costello RW; Maloney M; Atiyeh M; Gleich G; Walsh MT
[Ad] Endereço:Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland; E-Mails: rcostello@rcsi.ie (R.W.C.); micmaloney@rcsi.ie (M.M.); matiyeh@rcsi.ie (M.A.).
[Ti] Título:Mechanism of sphingosine 1-phosphate- and lysophosphatidic acid-induced up-regulation of adhesion molecules and eosinophil chemoattractant in nerve cells.
[So] Source:Int J Mol Sci;12(5):3237-49, 2011.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The lysophospholipids sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA) act via G-protein coupled receptors S1P(1-5) and LPA(1-3) respectively, and are implicated in allergy. Eosinophils accumulate at innervating cholinergic nerves in asthma and adhere to nerve cells via intercellular adhesion molecule-1 (ICAM-1). IMR-32 neuroblastoma cells were used as an in vitro cholinergic nerve cell model. The G(i) coupled receptors S1P(1), S1P(3), LPA(1), LPA(2) and LPA(3) were expressed on IMR-32 cells. Both S1P and LPA induced ERK phosphorylation and ERK- and G(i)-dependent up-regulation of ICAM-1 expression, with differing time courses. LPA also induced ERK- and G(i)-dependent up-regulation of the eosinophil chemoattractant, CCL-26. The eosinophil granule protein eosinophil peroxidase (EPO) induced ERK-dependent up-regulation of transcription of S1P(1), LPA(1), LPA(2) and LPA(3), providing the situation whereby eosinophil granule proteins may enhance S1P- and/or LPA- induced eosinophil accumulation at nerve cells in allergic conditions.
[Mh] Termos MeSH primário: Fatores Quimiotáticos de Eosinófilos/metabolismo
Lisofosfolipídeos/fisiologia
Neurônios/metabolismo
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Linhagem Celular
Seres Humanos
Receptores de Lisoesfingolipídeo/metabolismo
Receptores de Lisoesfingolipídeo/fisiologia
Transdução de Sinais
Esfingosina/fisiologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemotactic Factors, Eosinophil); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 26993-30-6 (sphingosine 1-phosphate); NGZ37HRE42 (Sphingosine); PG6M3969SG (lysophosphatidic acid)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110621
[St] Status:MEDLINE
[do] DOI:10.3390/ijms12053237


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[PMID]:20136617
[Au] Autor:Bae SJ; Lee JB; Shimizu K; Kuwazuka Y
[Ad] Endereço:Department of Dermatology, Nagasaki University, School of Medicine, Nagasaki, Japan.
[Ti] Título:Increase effect of transforming growth factor on eotaxin production by normal cultured dermal fibroblasts stimulated with interleukin-4: inhibitory effect of suplatast tosilate on eotaxin production.
[So] Source:Immunol Invest;39(2):93-102, 2010 Jan.
[Is] ISSN:1532-4311
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Eotaxin plays a central role in the development of allergic disease, including atopic dermatitis, asthma, and nasal allergy. Interleukin (IL)-4 induces eotaxin production in normal human dermal fibroblasts. On the other hands, Transforming growth factor-beta (TGF-beta), a multifunctional regulatory cytokine, affects many biological functions, including fibroblast growth and differentiation and Th2 cytokine regulation. In this study, we investigated the effect of TGF-beta on IL-4-induced eotaxin production by normal human fibroblasts, as well as the effect of suplatast tosilate, an antiallergic drug that selectively inhibits Th2 cytokine production. Dermal fibroblast treatment with IL-4 and TGF-beta for 24 h increased eotaxin production and expression of eotaxin mRNA, as measured by enzyme-linked immunosorbent assay (ELISA) and reverse-transcriptase polymerase chain reaction (RT-PCR), respectively. TGF-beta synergistically up-regulated eotaxin production and eotaxin mRNA expression when stimulated with IL-4. Suplatast tosilate dose-dependently inhibited eotaxin production induced by IL-4 or IL-4 plus TGF-beta. These results suggest that TGF-beta may regulate skin allergic inflammation by up-regulating eotaxin production in dermal fibroblasts. Suplatast tosilate might suppress this inflammation by inhibiting eotaxin production.
[Mh] Termos MeSH primário: Quimiocina CCL11
Fibroblastos/metabolismo
Fator de Crescimento Transformador beta/farmacologia
[Mh] Termos MeSH secundário: Antialérgicos/farmacologia
Sulfonatos de Arila/farmacologia
Asma/tratamento farmacológico
Asma/imunologia
Células Cultivadas
Quimiocina CCL11/antagonistas & inibidores
Quimiocina CCL11/biossíntese
Fatores Quimiotáticos de Eosinófilos/antagonistas & inibidores
Fatores Quimiotáticos de Eosinófilos/biossíntese
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Ensaio de Imunoadsorção Enzimática
Fibroblastos/efeitos dos fármacos
Fibroblastos/imunologia
Regulação da Expressão Gênica
Seres Humanos
Interleucina-4/farmacologia
Reação em Cadeia da Polimerase
RNA Mensageiro/antagonistas & inibidores
RNA Mensageiro/biossíntese
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Pele/citologia
Compostos de Sulfônio/farmacologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); 0 (Arylsulfonates); 0 (CCL11 protein, human); 0 (Chemokine CCL11); 0 (Chemotactic Factors, Eosinophil); 0 (RNA, Messenger); 0 (Sulfonium Compounds); 0 (Transforming Growth Factor beta); 207137-56-2 (Interleukin-4); C9J89787U1 (suplatast tosilate)
[Em] Mês de entrada:1008
[Cu] Atualização por classe:121115
[Lr] Data última revisão:
121115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100209
[St] Status:MEDLINE
[do] DOI:10.3109/08820130903496769


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[PMID]:19893035
[Au] Autor:Vieira AT; Fagundes CT; Alessandri AL; Castor MG; Guabiraba R; Borges VO; Silveira KD; Vieira EL; Gonçalves JL; Silva TA; Deruaz M; Proudfoot AE; Sousa LP; Teixeira MM
[Ad] Endereço:Laboratório de Imunofarmacologia, Colégio Técnico, Universidade Federal de Minas Gerais, Minas Gerais, Brazil,
[Ti] Título:Treatment with a novel chemokine-binding protein or eosinophil lineage-ablation protects mice from experimental colitis.
[So] Source:Am J Pathol;175(6):2382-91, 2009 Dec.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eosinophils are multifunctional leukocytes implicated in numerous inflammatory diseases. The present study was conducted to clarify the precise role of eosinophils in the development of colitis by using eosinophil-depleted mice and a novel chemokine-binding protein that neutralizes CCL11 action. Colitis was induced by administration of dextran sodium sulfate (DSS) to wild-type and eosinophil-deficient DeltadblGATA-1 mice. Accumulation of eosinophils in the gut of mice given DSS paralleled worsening of clinical score and weight loss. In response to DSS, DeltadblGATA-1 mice showed virtual absence of eosinophil recruitment, amelioration of clinical score, weight loss, and tissue destruction, and no lethality. There was a decrease in CXCL1 and CCL3 production and decreased neutrophil influx in the intestine of DeltadblGATA-1 mice. Transfer of bone marrow cells from wild-type mice reconstituted disease manifestation in DSS-treated DeltadblGATA-1 mice, and levels of CCL11 were increased after DSS treatment and localized to inflammatory cells. Treatment with the chemokine-binding protein evasin-4 at a dose that prevented the function of CCL11 greatly ameliorated clinical score, weight loss, overall tissue destruction, and death rates. In conclusion, the influx of eosinophils is critical for the induction of colitis by DSS. Treatment with a novel chemokine-binding protein decreased eosinophil influx and greatly ameliorated colitis, suggesting that strategies that interfere with the recruitment of eosinophils may be useful as therapy for colitis.
[Mh] Termos MeSH primário: Quimiocina CCL11/imunologia
Colite/imunologia
Eosinófilos/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Inibição de Migração Celular/imunologia
Fatores Quimiotáticos de Eosinófilos/antagonistas & inibidores
Quimiotaxia de Leucócito/imunologia
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos BALB C
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL11); 0 (Chemotactic Factors, Eosinophil)
[Em] Mês de entrada:1002
[Cu] Atualização por classe:141204
[Lr] Data última revisão:
141204
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:091107
[St] Status:MEDLINE
[do] DOI:10.2353/ajpath.2009.090093


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[PMID]:19505393
[Au] Autor:Ventura MT; Carretta A; Tummolo RA; Buquicchio R; Arsieni A; Murgia N
[Ad] Endereço:Department of Internal Medicine, Immunology and Infectious Diseases MIDIM, University of Bari Medical School, Policlinico, Bari, Italy. mt.ventura@allergy.uniba.it
[Ti] Título:Clinical data and inflammation parameters in patients with cypress allergy treated with sublingual swallow therapy and subcutaneous immunotherapy.
[So] Source:Int J Immunopathol Pharmacol;22(2):403-13, 2009 Apr-Jun.
[Is] ISSN:0394-6320
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The clinical efficacy of immunotherapy, either by high dose sublingual-swallow therapy (SLIT) or subcutaneous immunotherapy (SCIT), has been demonstrated in patients with pollinosis but few studies have been carried out analysing differences in these treatments in terms of an improvement of clinical and allergic phlogosis parameters. The aim of this double-blind placebo-controlled study is to investigate the efficacy of high dose SLIT and SCIT using a purified standardized Juniperus ashei extract in a population of allergic patients monosensitized to cypress. Forty patients with cypress-allergic rhino conjunctivitis were administered therapeutic or placebo SLIT or SCIT for 12 months. Laboratory parameters were studied, namely the eosinophil cationic protein (ECP) level in nasal lavage and in serum, as well as the number of eosinophils (EOS) in peripheral blood and in nasal lavage and the level of eosinophil chemotactic activity (ECA). These parameters were correlated with clinical symptoms, evaluated by means of the clinical symptoms score (CSS). After SCIT and SLIT the levels of ECP and ECA were reduced in nasal lavage. We also observed a significant reduction in the values of ECP in serum in the patients treated with SLIT. EOS were unchanged in peripheral blood, but significantly reduced in nasal lavage. These data were in accordance with the improvement of clinical symptoms, supported by the close correlation between CSS and laboratory parameters. Our data confirm a clinical improvement correlated with a decline in inflammation parameters after one year of immunotherapy, supporting the hypothesis that treatment with a major allergen of cypress is able to change the course of allergic rhinitis.
[Mh] Termos MeSH primário: Antígenos de Plantas/administração & dosagem
Conjuntivite Alérgica/terapia
Cupressus/imunologia
Dessensibilização Imunológica/métodos
Eosinófilos/imunologia
Mediadores da Inflamação/sangue
Pólen/imunologia
Rinite Alérgica Sazonal/terapia
[Mh] Termos MeSH secundário: Administração Sublingual
Adolescente
Adulto
Antígenos de Plantas/imunologia
Fatores Quimiotáticos de Eosinófilos/metabolismo
Quimiotaxia de Leucócito
Conjuntivite Alérgica/imunologia
Método Duplo-Cego
Proteína Catiônica de Eosinófilo/sangue
Feminino
Seres Humanos
Injeções Subcutâneas
Contagem de Leucócitos
Masculino
Meia-Idade
Líquido da Lavagem Nasal/citologia
Líquido da Lavagem Nasal/imunologia
Rinite Alérgica Sazonal/imunologia
Fatores de Tempo
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antigens, Plant); 0 (Chemotactic Factors, Eosinophil); 0 (Inflammation Mediators); EC 3.1.27.- (Eosinophil Cationic Protein); EC 3.1.27.- (RNASE3 protein, human)
[Em] Mês de entrada:0907
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090610
[St] Status:MEDLINE


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[PMID]:19141355
[Au] Autor:Aceves SS; Ackerman SJ
[Ad] Endereço:Division of Allergy and Immunology, Rady Children's Hospital, 3020 Children's Way, MC 5114, San Diego, CA 92123-6791, USA.
[Ti] Título:Relationships between eosinophilic inflammation, tissue remodeling, and fibrosis in eosinophilic esophagitis.
[So] Source:Immunol Allergy Clin North Am;29(1):197-211, xiii-xiv, 2009 Feb.
[Is] ISSN:1557-8607
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The clinical and pathologic features of eosinophilic esophagitis (EE) include extensive tissue remodeling. Increasing evidence supports a key role for the eosinophil in multiple aspects of the esophageal remodeling and fibrosis seen in this allergic disease. This article reviews the clinical implications of esophageal remodeling and fibrosis in EE and discusses the possible pathogenic mechanisms inducing and regulating these responses. The focus is specifically on eosinophil and cytokine interactions with the esophageal epithelium, vascular endothelium, resident fibroblasts, and smooth muscle. Current and potential therapeutic interventions are discussed that may impact the development or resolution of chronic esophageal remodeling and fibrosis in EE.
[Mh] Termos MeSH primário: Eosinofilia/imunologia
Eosinófilos/metabolismo
Esofagite/imunologia
Hipersensibilidade/imunologia
Mucosa Intestinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Comunicação Celular
Movimento Celular
Sobrevivência Celular
Fatores Quimiotáticos de Eosinófilos/imunologia
Células Endoteliais/imunologia
Células Endoteliais/metabolismo
Células Endoteliais/patologia
Eosinofilia/complicações
Eosinofilia/metabolismo
Eosinofilia/patologia
Eosinófilos/imunologia
Eosinófilos/patologia
Esofagite/complicações
Esofagite/metabolismo
Esofagite/patologia
Fibroblastos/imunologia
Fibroblastos/metabolismo
Fibroblastos/patologia
Fibrose/imunologia
Seres Humanos
Hipersensibilidade/complicações
Hipersensibilidade/metabolismo
Hipersensibilidade/patologia
Inflamação
Mucosa Intestinal/imunologia
Mucosa Intestinal/patologia
Fatores de Crescimento Neural/imunologia
Fator de Crescimento Transformador beta/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Chemotactic Factors, Eosinophil); 0 (Nerve Growth Factors); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:0910
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090115
[St] Status:MEDLINE
[do] DOI:10.1016/j.iac.2008.10.003


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[PMID]:19141354
[Au] Autor:Wershil BK
[Ad] Endereço:Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital, 2300 Children's Plaza, Box 65, Chicago, IL 60614, USA. bwershil@childrensmemorial.org
[Ti] Título:Exploring the role of mast cells in eosinophilic esophagitis.
[So] Source:Immunol Allergy Clin North Am;29(1):189-95, xiii, 2009 Feb.
[Is] ISSN:1557-8607
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mast cell plays a critical role in allergic responses in the gastrointestinal tract and other sites. Emerging evidence indicates that mast cells also participate in the pathogenesis of eosinophilic esophagitis, although their precise role has not been defined. This article reviews the biology of mast cells and examines the potential involvement of the cell as an effector of the inflammatory response and tissue remodeling, and as a cell that has the potential to function as an immunomodulator and limit inflammation.
[Mh] Termos MeSH primário: Degranulação Celular/imunologia
Eosinofilia/patologia
Esofagite/patologia
Hipersensibilidade/patologia
Mastócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Movimento Celular/imunologia
Fatores Quimiotáticos de Eosinófilos/metabolismo
Proteínas do Sistema Complemento/metabolismo
Eosinofilia/complicações
Eosinofilia/imunologia
Esofagite/complicações
Esofagite/imunologia
Seres Humanos
Hipersensibilidade/complicações
Hipersensibilidade/imunologia
Mastócitos/imunologia
Mastócitos/patologia
Receptores Toll-Like/genética
Receptores Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chemotactic Factors, Eosinophil); 0 (Toll-Like Receptors); 0 (Tumor Necrosis Factor-alpha); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:0910
[Cu] Atualização por classe:090114
[Lr] Data última revisão:
090114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090115
[St] Status:MEDLINE
[do] DOI:10.1016/j.iac.2008.09.006


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[PMID]:19141339
[Au] Autor:Mishra A
[Ad] Endereço:Department of Pediatrics, Division of Allergy and Immunology, 3333 Burnnet Avenue, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, OH 45229, USA. anil.mishra@cchmc.org
[Ti] Título:Mechanism of eosinophilic esophagitis.
[So] Source:Immunol Allergy Clin North Am;29(1):29-40, viii, 2009 Feb.
[Is] ISSN:1557-8607
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eosinophilic esophagitis (EoE) is a newly recognized disease and is an emerging entity throughout developing and developed countries, including the United States. Therefore, understanding the causes, natural history, diagnosis, and management is important for future therapeutic interventions. The pathogenesis of EoE is still not clear, but a growing body of evidence has established that this condition represents a T-cell-mediated immune response involving several proinflammatory mediators and chemoattractants known to regulate eosinophilic accumulation in the esophagus, such as IL-4, IL-5, IL-3 and eotaxin-1, -2, and -3. Determining the mechanism or mechanisms through which human esophageal-derived factors ultimately induce the functional abnormalities observed, and to which antigens patients who have EoE are sensitized that lead to the manifestation of symptoms, is of significant interest.
[Mh] Termos MeSH primário: Fatores Quimiotáticos de Eosinófilos/imunologia
Eosinófilos/metabolismo
Hipersensibilidade Alimentar/imunologia
Hipersensibilidade Respiratória/imunologia
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Alérgenos/imunologia
Animais
Anticorpos Monoclonais/uso terapêutico
Dietoterapia
Eosinofilia/diagnóstico
Eosinofilia/etiologia
Eosinofilia/patologia
Eosinofilia/fisiopatologia
Eosinofilia/terapia
Eosinófilos/imunologia
Eosinófilos/patologia
Esofagite/diagnóstico
Esofagite/etiologia
Esofagite/patologia
Esofagite/fisiopatologia
Esofagite/terapia
Hipersensibilidade Alimentar/complicações
Glucocorticoides/uso terapêutico
Seres Humanos
Imunidade Celular
Interleucina-5/imunologia
Hipersensibilidade Respiratória/complicações
Linfócitos T/imunologia
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Allergens); 0 (Antibodies, Monoclonal); 0 (Chemotactic Factors, Eosinophil); 0 (Glucocorticoids); 0 (Interleukin-5)
[Em] Mês de entrada:0910
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090115
[St] Status:MEDLINE
[do] DOI:10.1016/j.iac.2008.09.010


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[PMID]:18187208
[Au] Autor:Turner DG; Wildblood LA; Inglis NF; Jones DG
[Ad] Endereço:Moredun Research Institute, Pentlands Science Park, Bush Loan, Penicuik EH26 0PZ, Scotland, UK. darryl.turner@moredun.ac.uk
[Ti] Título:Characterization of a galectin-like activity from the parasitic nematode, Haemonchus contortus, which modulates ovine eosinophil migration in vitro.
[So] Source:Vet Immunol Immunopathol;122(1-2):138-45, 2008 Mar 15.
[Is] ISSN:0165-2427
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The development of eosinophilia is a characteristic feature of helminth infection, although the exact nature of the interaction between eosinophils and parasites remains to be fully defined. Previously, it has been reported that Haemonchus contortus and other nematodes produce eosinophil-specific chemoattractants. This paper describes studies aimed at isolating and identifying the factor(s) responsible. Initial studies showed that soluble extracts of infective larvae (L3) of H. contortus provoked a chemokinetic, rather than chemotactic, response in ovine bone marrow eosinophils in vitro. This activity was inhibited by lactose to a markedly greater extent than sucrose suggesting a galectin-like identity. Lactose affinity chromatography of soluble H. contortus extracts resulted in the isolation a specific bound fraction which retained biological activity. SDS-PAGE gel electrophoresis indicated a single Coomassie-stained band at between 31 and 41kDa. Subsequent, mass spectrometric analysis confirmed that the bound fraction contained a mixture of nematode galectins. The results confirm that H. contortus larvae produce several galectin-like proteins, at least one of which demonstrates eosinophil chemokinetic activity in vitro. The possibility of the parasite-derived factor mimicking the mammalian galectin-9, a known eosinophil chemokine, is discussed.
[Mh] Termos MeSH primário: Fatores Quimiotáticos de Eosinófilos/fisiologia
Galectinas/fisiologia
Haemonchus/fisiologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Movimento Celular
Fatores Quimiotáticos de Eosinófilos/análise
Quimiotaxia
Eosinófilos/fisiologia
Lactose/metabolismo
Lactose/farmacologia
Dados de Sequência Molecular
Ovinos
Espectrometria de Massas por Ionização por Electrospray
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemotactic Factors, Eosinophil); 0 (Galectins); J2B2A4N98G (Lactose)
[Em] Mês de entrada:0804
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080112
[St] Status:MEDLINE
[do] DOI:10.1016/j.vetimm.2007.11.002



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