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Dexamethasone Inhibits Tumor Necrosis Factor-α-Induced Expression of Macrophage Inflammatory Protein-2 and Adhesion of Neutrophils to Endothelial Cells
- Source :
- Biochemical and Biophysical Research Communications. 271:364-367
- Publication Year :
- 2000
- Publisher :
- Elsevier BV, 2000.
-
Abstract
- Macrophage inflammatory protein-2 (MIP-2) belongs to the C-X-C subfamily of chemokines and appears to play an important role in cytokine-induced inflammatory and immune cell-mediated responses. We found that tumor necrosis factor-alpha (TNF-alpha) time- and dose-dependently increased gene and protein expression of MIP-2 in endothelial cells. Moreover, it was observed that dexamethasone treatment inhibited endothelial cell expression of MIP-2 in response to TNF-alpha stimulation and markedly reduced the number of adherent neutrophils. Moreover, we found that a monoclonal antibody against murine MIP-2 abolished neutrophil adhesion to TNF-alpha-activated endothelial cells. These data demonstrate that TNF-alpha induces expression of MIP-2 in endothelial cells and support the hypothesis that the anti-inflammatory action of dexamethasone may, at least in part, be attributable to an inhibition of MIP-2 induction on cytokine-activated endothelial cells.
- Subjects :
- Chemokine
Time Factors
Antineoplastic Agents, Hormonal
Endothelium
Neutrophils
medicine.drug_class
Chemokine CXCL2
Biophysics
Enzyme-Linked Immunosorbent Assay
Vascular endothelial growth inhibitor
Monoclonal antibody
Biochemistry
Dexamethasone
Mice
Immune system
Cell Adhesion
medicine
Animals
Humans
Macrophage
Molecular Biology
Cell Line, Transformed
Inflammation
Dose-Response Relationship, Drug
biology
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha
Chemistry
Monokines
Cell Biology
Molecular biology
Mice, Inbred C57BL
Endothelial stem cell
medicine.anatomical_structure
biology.protein
Tumor necrosis factor alpha
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 271
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....6259f52043411ea0378598203d9fc416