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Campo DC | Valor | Idioma |
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dc.contributor.author | Manfredo Vieira, Silvio | - |
dc.contributor.author | Lemos, Henrique Paula | - |
dc.contributor.author | Grespan, Renata | - |
dc.contributor.author | Napimoga, Marcelo Henrique | - |
dc.contributor.author | Dal-Secco, Daniela | - |
dc.contributor.author | Freitas, Andressa de | - |
dc.contributor.author | Cunha, Thiago Mattar | - |
dc.contributor.author | Verri, Waldiceu A. | - |
dc.contributor.author | Souza, Devandir Antonio | - |
dc.contributor.author | Jamur, Maria Célia | - |
dc.contributor.author | Fernandes, Karla S. | - |
dc.contributor.author | Oliver, Constance | - |
dc.contributor.author | Silva, Joäo Santana da | - |
dc.contributor.author | Teixeira, Mauro Martins | - |
dc.contributor.author | Cunha, Fernando Queiroz | - |
dc.date.accessioned | 2020-06-15T21:54:38Z | - |
dc.date.available | 2020-06-15T21:54:38Z | - |
dc.date.issued | 2009 | - |
dc.identifier.uri | https://repositorio.inpa.gov.br/handle/1/18410 | - |
dc.description.abstract | Background and purpose: Chemokines orchestrate neutrophil recruitment to inflammatory foci. In the present study, we evaluated the participation of three chemokines, KC/CXCL1, MIP-2/CXCL2 and LIX/CXCL5, which are ligands for chemokine receptor 2 (CXCR2), in mediating neutrophil recruitment in immune inflammation induced by antigen in immunized mice. Experimental approach: Neutrophil recruitment was assessed in immunized mice challenged with methylated bovine serum albumin, KC/CXCL1, LIX/CXCL5 or tumour necrosis factor (TNF)-α. Cytokine and chemokine levels were determined in peritoneal exudates and in supernatants of macrophages and mast cells by elisa. CXCR2 and intercellular adhesion molecule 1 (ICAM-1) expression was determined using immunohistochemistry and confocal microscopy. Key results: Antigen challenge induced dose- and time-dependent neutrophil recruitment and production of KC/CXCL1, LIX/CXCL5 and TNF-α, but not MIP-2/CXCL2, in peritoneal exudates. Neutrophil recruitment was inhibited by treatment with reparixin (CXCR1/2 antagonist), anti-KC/CXCL1, anti-LIX/CXCL5 or anti-TNF-α antibodies and in tumour necrosis factor receptor 1-deficient mice. Intraperitoneal injection of KC/CXCL1 and LIX/CXCL5 induced dose- and time-dependent neutrophil recruitment and TNF-α production, which were inhibited by reparixin or anti-TNF-α treatment. Macrophages and mast cells expressed CXCR2 receptors. Increased macrophage numbers enhanced, while cromolyn sodium (mast cell stabilizer) diminished, LIX/CXCL5-induced neutrophil recruitment. Macrophages and mast cells from immunized mice produced TNF-α upon LIX/CXCL5 stimulation. Methylated bovine serum albumin induced expression of ICAM-1 on mesenteric vascular endothelium, which was inhibited by anti-TNF-α or anti-LIX/CXCL5. Conclusion and implications: Following antigen challenge, CXCR2 ligands are produced and act on macrophages and mast cells triggering the production of TNF-α, which synergistically contribute to neutrophil recruitment through induction of the expression of ICAM-1. © 2009 The British Pharmacological Society. | en |
dc.language.iso | en | pt_BR |
dc.relation.ispartof | Volume 158, Número 3, Pags. 779-789 | pt_BR |
dc.rights | Restrito | * |
dc.subject | 3 [3 Tert Butylthio 1 (4 Chlorobenzyl) 5 Isopropyl 2 Indolyl] 2,2 Dimethylpropionic Acid | en |
dc.subject | Antigen | en |
dc.subject | Serum Albumin, Bovine | en |
dc.subject | Chemokine Receptor Antagonist | en |
dc.subject | Chemokine Receptor Ccr2 | en |
dc.subject | Chemokine Receptor Cxcr1 | en |
dc.subject | Chemokine Receptor Cxcr2 | en |
dc.subject | Cromoglycate Disodium | en |
dc.subject | Cxcl1 Chemokine | en |
dc.subject | Cxcl1 Chemokine Antibody | en |
dc.subject | Cxcl2 Chemokine | en |
dc.subject | Cytokine | en |
dc.subject | Cytokine Antibody | en |
dc.subject | Epithelial Derived Neutrophil Activating Factor 78 | en |
dc.subject | Epithelial Derived Neutrophil Activating Factor 78 Antibody | en |
dc.subject | Intercellular Adhesion Molecule-1 | en |
dc.subject | Ligand | en |
dc.subject | Reparixin | en |
dc.subject | Stabilizing Agent | en |
dc.subject | Tumor Necrosis Factor-alpha | en |
dc.subject | Tumor Necrosis Factor Alpha Antibody | en |
dc.subject | Tumor Necrosis Factor Receptor 1 | en |
dc.subject | Unclassified Drug | en |
dc.subject | Animals Cell | en |
dc.subject | Animals Experiment | en |
dc.subject | Animals Model | en |
dc.subject | Animals Tissue | en |
dc.subject | Confocal Microscopy | en |
dc.subject | Controlled Study | en |
dc.subject | Dose Time Effect Relation | en |
dc.subject | Enzyme-linked Immunosorbent Assay | en |
dc.subject | Immunization | en |
dc.subject | Immunohistochemistry | en |
dc.subject | Inflammation | en |
dc.subject | Macrophage | en |
dc.subject | Mast Cell | en |
dc.subject | Mesenteric Vein | en |
dc.subject | Methylation | en |
dc.subject | Mouse | en |
dc.subject | Neutrophil Chemotaxis | en |
dc.subject | Nonhuman | en |
dc.subject | Peritoneum Exudate | en |
dc.subject | Priority Journal | en |
dc.subject | Protein Expression | en |
dc.subject | Supernatant | en |
dc.subject | Vascular Endothelium | en |
dc.subject | Animal | en |
dc.subject | Antibodies | en |
dc.subject | Cattle | en |
dc.subject | Cxcl1 Chemokine | en |
dc.subject | Chemokine Cxcl5 | en |
dc.subject | Intercellular Adhesion Molecule-1 | en |
dc.subject | Macrophages, Peritoneal | en |
dc.subject | Mast Cells | en |
dc.subject | Mice | en |
dc.subject | Mice, Inbred Balb C | en |
dc.subject | Mice, Inbred C57bl | en |
dc.subject | Mice, Knockout | en |
dc.subject | Neutrophils | en |
dc.subject | Peritonitis | en |
dc.subject | Receptors, Interleukin-8a | en |
dc.subject | Receptors, Interleukin-8b | en |
dc.subject | Receptors, Tumor Necrosis Factor, Type I | en |
dc.subject | Serum Albumin | en |
dc.subject | Sulfonamides | en |
dc.subject | Tumor Necrosis Factor-alpha | en |
dc.title | A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER | en |
dc.type | Artigo | pt_BR |
dc.identifier.doi | 10.1111/j.1476-5381.2009.00367.x | - |
dc.publisher.journal | British Journal of Pharmacology | pt_BR |
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