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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/70291
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dc.contributor.authorOliveira, Sandra Helena Penha de-
dc.contributor.authorCanetti, C.-
dc.contributor.authorRibeiro, R. A.-
dc.contributor.authorCunha, F. Q.-
dc.date.accessioned2014-05-27T11:22:48Z-
dc.date.accessioned2016-10-25T18:25:11Z-
dc.date.available2014-05-27T11:22:48Z-
dc.date.available2016-10-25T18:25:11Z-
dc.date.issued2008-02-01-
dc.identifierhttp://dx.doi.org/10.1007/s10753-007-9047-x-
dc.identifier.citationInflammation, v. 31, n. 1, p. 36-46, 2008.-
dc.identifier.issn0360-3997-
dc.identifier.urihttp://hdl.handle.net/11449/70291-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/70291-
dc.description.abstractIn the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1β-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1β induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB 4, PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1β-induced neutrophil migration. The neutrophil migration induced by IL-1β is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1β released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1β. The chemotactic activity of the supernatant of IL-1β-stimulated macrophages is due to the presence of LTB4, since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1β-stimulated mast cells supernatant is due to the presence of IL-1β and TNF-α, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion, our results suggest that neutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon IL-1β and TNFα released by mast cells. © 2007 Springer Science+Business Media, LLC.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ)-
dc.format.extent36-46-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectIL-1β-
dc.subjectLTB4-
dc.subjectMast cells-
dc.subjectNeutrophil migration-
dc.subjectTNF-α-
dc.subject1,4 dihydro 2,4,6 trimethyl 3,5 pyridinedicarboxylic acid methyl 2 phenylthioethyl ester-
dc.subject3 [3 tert butylthio 1 (4 chlorobenzyl) 5 isopropyl 2 indolyl] 2,2 dimethylpropionic acid-
dc.subjectdexamethasone-
dc.subjectinterleukin 1beta-
dc.subjectleukotriene B4-
dc.subjectthrombocyte activating factor-
dc.subjecttumor necrosis factor alpha-
dc.subjectanimal cell-
dc.subjectanimal experiment-
dc.subjectcell stimulation-
dc.subjectconcentration response-
dc.subjectcontrolled study-
dc.subjectmacrophage-
dc.subjectmale-
dc.subjectmast cell-
dc.subjectneutrophil-
dc.subjectneutrophil chemotaxis-
dc.subjectnonhuman-
dc.subjectperitoneal cavity-
dc.subjectprotein analysis-
dc.subjectprotein function-
dc.subjectprotein secretion-
dc.subjectrat-
dc.subjectAnimals-
dc.subjectAnti-Inflammatory Agents-
dc.subjectArachidonate 5-Lipoxygenase-
dc.subjectCell Movement-
dc.subjectInterleukin-1beta-
dc.subjectLeukotriene B4-
dc.subjectMacrophages-
dc.subjectMacrophages, Peritoneal-
dc.subjectMale-
dc.subjectMast Cells-
dc.subjectModels, Biological-
dc.subjectNeutrophils-
dc.subjectRats-
dc.subjectRats, Wistar-
dc.subjectTumor Necrosis Factor-alpha-
dc.subjectAnimalia-
dc.subjectRattus-
dc.titleNeutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon TNF-α and IL-1β released by mast cellsen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionFederal University of Rio de Janeiro-
dc.contributor.institutionFederal University of Ceará-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationDepartment of Basic Science School of Dentistry Sao Paulo State University, Rua José Bonifácio, 1193, 16015-050 Araçatuba, Sao Paulo-
dc.description.affiliationInstitute of Biophysics Carlos Chagas Filho Federal University of Rio de Janeiro, Rio de Janeiro-
dc.description.affiliationDepartment of Physiology and Pharmacology Faculty of Medicine Federal University of Ceará, Fortaleza, Ceará-
dc.description.affiliationDepartment of Pharmacology Faculty of Medicine of Ribeirão Preto University of São Paulo, Ribeirão Preto, São Paulo-
dc.description.affiliationUnespDepartment of Basic Science School of Dentistry Sao Paulo State University, Rua José Bonifácio, 1193, 16015-050 Araçatuba, Sao Paulo-
dc.identifier.doi10.1007/s10753-007-9047-x-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofInflammation-
dc.identifier.scopus2-s2.0-39049112964-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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