A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER
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...
| Autor principal: | Manfredo Vieira, Silvio |
|---|---|
| Outros Autores: | Lemos, Henrique Paula, Grespan, Renata, Napimoga, Marcelo Henrique, Dal-Secco, Daniela, Freitas, Andressa de, Cunha, Thiago Mattar, Verri, Waldiceu A., Souza, Devandir Antonio, Jamur, Maria Célia, Fernandes, Karla S., Oliver, Constance, Silva, Joäo Santana da, Teixeira, Mauro Martins, Cunha, Fernando Queiroz |
| Grau: | Artigo |
| Idioma: | English |
| Publicado em: |
British Journal of Pharmacology
2020
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https://repositorio.inpa.gov.br/handle/1/18410 |
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oai:repositorio:1-18410 A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER Manfredo Vieira, Silvio Lemos, Henrique Paula Grespan, Renata Napimoga, Marcelo Henrique Dal-Secco, Daniela Freitas, Andressa de Cunha, Thiago Mattar Verri, Waldiceu A. Souza, Devandir Antonio Jamur, Maria Célia Fernandes, Karla S. Oliver, Constance Silva, Joäo Santana da Teixeira, Mauro Martins Cunha, Fernando Queiroz 3 [3 Tert Butylthio 1 (4 Chlorobenzyl) 5 Isopropyl 2 Indolyl] 2,2 Dimethylpropionic Acid Antigen Serum Albumin, Bovine Chemokine Receptor Antagonist Chemokine Receptor Ccr2 Chemokine Receptor Cxcr1 Chemokine Receptor Cxcr2 Cromoglycate Disodium Cxcl1 Chemokine Cxcl1 Chemokine Antibody Cxcl2 Chemokine Cytokine Cytokine Antibody Epithelial Derived Neutrophil Activating Factor 78 Epithelial Derived Neutrophil Activating Factor 78 Antibody Intercellular Adhesion Molecule-1 Ligand Reparixin Stabilizing Agent Tumor Necrosis Factor-alpha Tumor Necrosis Factor Alpha Antibody Tumor Necrosis Factor Receptor 1 Unclassified Drug Animals Cell Animals Experiment Animals Model Animals Tissue Confocal Microscopy Controlled Study Dose Time Effect Relation Enzyme-linked Immunosorbent Assay Immunization Immunohistochemistry Inflammation Macrophage Mast Cell Mesenteric Vein Methylation Mouse Neutrophil Chemotaxis Nonhuman Peritoneum Exudate Priority Journal Protein Expression Supernatant Vascular Endothelium Animal Antibodies Cattle Cxcl1 Chemokine Chemokine Cxcl5 Intercellular Adhesion Molecule-1 Macrophages, Peritoneal Mast Cells Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Neutrophils Peritonitis Receptors, Interleukin-8a Receptors, Interleukin-8b Receptors, Tumor Necrosis Factor, Type I Serum Albumin Sulfonamides Tumor Necrosis Factor-alpha 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. 2020-06-15T21:54:38Z 2020-06-15T21:54:38Z 2009 Artigo https://repositorio.inpa.gov.br/handle/1/18410 10.1111/j.1476-5381.2009.00367.x en Volume 158, Número 3, Pags. 779-789 Restrito British Journal of Pharmacology |
| institution |
Instituto Nacional de Pesquisas da Amazônia - Repositório Institucional |
| collection |
INPA-RI |
| language |
English |
| topic |
3 [3 Tert Butylthio 1 (4 Chlorobenzyl) 5 Isopropyl 2 Indolyl] 2,2 Dimethylpropionic Acid Antigen Serum Albumin, Bovine Chemokine Receptor Antagonist Chemokine Receptor Ccr2 Chemokine Receptor Cxcr1 Chemokine Receptor Cxcr2 Cromoglycate Disodium Cxcl1 Chemokine Cxcl1 Chemokine Antibody Cxcl2 Chemokine Cytokine Cytokine Antibody Epithelial Derived Neutrophil Activating Factor 78 Epithelial Derived Neutrophil Activating Factor 78 Antibody Intercellular Adhesion Molecule-1 Ligand Reparixin Stabilizing Agent Tumor Necrosis Factor-alpha Tumor Necrosis Factor Alpha Antibody Tumor Necrosis Factor Receptor 1 Unclassified Drug Animals Cell Animals Experiment Animals Model Animals Tissue Confocal Microscopy Controlled Study Dose Time Effect Relation Enzyme-linked Immunosorbent Assay Immunization Immunohistochemistry Inflammation Macrophage Mast Cell Mesenteric Vein Methylation Mouse Neutrophil Chemotaxis Nonhuman Peritoneum Exudate Priority Journal Protein Expression Supernatant Vascular Endothelium Animal Antibodies Cattle Cxcl1 Chemokine Chemokine Cxcl5 Intercellular Adhesion Molecule-1 Macrophages, Peritoneal Mast Cells Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Neutrophils Peritonitis Receptors, Interleukin-8a Receptors, Interleukin-8b Receptors, Tumor Necrosis Factor, Type I Serum Albumin Sulfonamides Tumor Necrosis Factor-alpha |
| spellingShingle |
3 [3 Tert Butylthio 1 (4 Chlorobenzyl) 5 Isopropyl 2 Indolyl] 2,2 Dimethylpropionic Acid Antigen Serum Albumin, Bovine Chemokine Receptor Antagonist Chemokine Receptor Ccr2 Chemokine Receptor Cxcr1 Chemokine Receptor Cxcr2 Cromoglycate Disodium Cxcl1 Chemokine Cxcl1 Chemokine Antibody Cxcl2 Chemokine Cytokine Cytokine Antibody Epithelial Derived Neutrophil Activating Factor 78 Epithelial Derived Neutrophil Activating Factor 78 Antibody Intercellular Adhesion Molecule-1 Ligand Reparixin Stabilizing Agent Tumor Necrosis Factor-alpha Tumor Necrosis Factor Alpha Antibody Tumor Necrosis Factor Receptor 1 Unclassified Drug Animals Cell Animals Experiment Animals Model Animals Tissue Confocal Microscopy Controlled Study Dose Time Effect Relation Enzyme-linked Immunosorbent Assay Immunization Immunohistochemistry Inflammation Macrophage Mast Cell Mesenteric Vein Methylation Mouse Neutrophil Chemotaxis Nonhuman Peritoneum Exudate Priority Journal Protein Expression Supernatant Vascular Endothelium Animal Antibodies Cattle Cxcl1 Chemokine Chemokine Cxcl5 Intercellular Adhesion Molecule-1 Macrophages, Peritoneal Mast Cells Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Neutrophils Peritonitis Receptors, Interleukin-8a Receptors, Interleukin-8b Receptors, Tumor Necrosis Factor, Type I Serum Albumin Sulfonamides Tumor Necrosis Factor-alpha Manfredo Vieira, Silvio A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER |
| topic_facet |
3 [3 Tert Butylthio 1 (4 Chlorobenzyl) 5 Isopropyl 2 Indolyl] 2,2 Dimethylpropionic Acid Antigen Serum Albumin, Bovine Chemokine Receptor Antagonist Chemokine Receptor Ccr2 Chemokine Receptor Cxcr1 Chemokine Receptor Cxcr2 Cromoglycate Disodium Cxcl1 Chemokine Cxcl1 Chemokine Antibody Cxcl2 Chemokine Cytokine Cytokine Antibody Epithelial Derived Neutrophil Activating Factor 78 Epithelial Derived Neutrophil Activating Factor 78 Antibody Intercellular Adhesion Molecule-1 Ligand Reparixin Stabilizing Agent Tumor Necrosis Factor-alpha Tumor Necrosis Factor Alpha Antibody Tumor Necrosis Factor Receptor 1 Unclassified Drug Animals Cell Animals Experiment Animals Model Animals Tissue Confocal Microscopy Controlled Study Dose Time Effect Relation Enzyme-linked Immunosorbent Assay Immunization Immunohistochemistry Inflammation Macrophage Mast Cell Mesenteric Vein Methylation Mouse Neutrophil Chemotaxis Nonhuman Peritoneum Exudate Priority Journal Protein Expression Supernatant Vascular Endothelium Animal Antibodies Cattle Cxcl1 Chemokine Chemokine Cxcl5 Intercellular Adhesion Molecule-1 Macrophages, Peritoneal Mast Cells Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Neutrophils Peritonitis Receptors, Interleukin-8a Receptors, Interleukin-8b Receptors, Tumor Necrosis Factor, Type I Serum Albumin Sulfonamides Tumor Necrosis Factor-alpha |
| description |
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. |
| format |
Artigo |
| author |
Manfredo Vieira, Silvio |
| author2 |
Lemos, Henrique Paula Grespan, Renata Napimoga, Marcelo Henrique Dal-Secco, Daniela Freitas, Andressa de Cunha, Thiago Mattar Verri, Waldiceu A. Souza, Devandir Antonio Jamur, Maria Célia Fernandes, Karla S. Oliver, Constance Silva, Joäo Santana da Teixeira, Mauro Martins Cunha, Fernando Queiroz |
| author2Str |
Lemos, Henrique Paula Grespan, Renata Napimoga, Marcelo Henrique Dal-Secco, Daniela Freitas, Andressa de Cunha, Thiago Mattar Verri, Waldiceu A. Souza, Devandir Antonio Jamur, Maria Célia Fernandes, Karla S. Oliver, Constance Silva, Joäo Santana da Teixeira, Mauro Martins Cunha, Fernando Queiroz |
| 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 |
| title_short |
A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER |
| title_full |
A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER |
| title_fullStr |
A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER |
| title_full_unstemmed |
A crucial role for TNF-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5: RESEARCH PAPER |
| title_sort |
crucial role for tnf-α in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, kc/cxcl1 and lix/cxcl5: research paper |
| publisher |
British Journal of Pharmacology |
| publishDate |
2020 |
| url |
https://repositorio.inpa.gov.br/handle/1/18410 |
| _version_ |
1787142970459291648 |
| score |
11.675088 |