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Chemokine amplification in mesangial cells.
Y Luo1, C Lloyd, J C Gutierrez-Ramos
1Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|September 22, 1999
Summary
Macrophage inflammatory protein-2 (MIP-2) and KC chemokines drive mesangial cell migration and chemokine production. This self-stimulating cascade may worsen chronic glomerular inflammation.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Mesangial cells are key in glomerular nephritis pathogenesis.
- These cells share traits with smooth muscle cells and macrophages.
- Chemokines play a role in inflammatory responses within the kidney.
Purpose of the Study:
- To investigate the effect of CXC-chemokines MIP-2 and KC on mouse mesangial cells.
- To explore the potential for a chemokine feedback loop in mesangial cells.
- To determine if these effects are specific to mesangial cells.
Main Methods:
- Treatment of mouse mesangial cells with MIP-2 and KC.
- Analysis of chemokine gene and protein expression (MCP-1, RANTES, MIP-2, KC).
- Comparison of mesangial cell responses with renal cortical epithelial cells and peritoneal macrophages.
Main Results:
- MIP-2 and KC induced mesangial cell migration.
- Treatment upregulated monocyte chemoattractant protein-1 and RANTES.
- Autoinduction of MIP-2 and KC mRNA was observed.
- These chemokines did not induce chemokine production in epithelial cells or macrophages.
- Higher doses induced MIP-1alpha, MIP-1beta, and IFN-gamma-inducible protein-10.
Conclusions:
- Mesangial cells exhibit a unique chemokine feedback mechanism involving MIP-2 and KC.
- This chemokine cascade may promote leukocyte infiltration and activation in the glomerulus.
- Self-stimulation of chemokines by mesangial cells could contribute to chronic glomerular inflammation.