Correlative insights into immunoexpression of monocyte chemoattractant protein-1, transforming growth factor beta-1...

The experimental data and the study on human renal tissue in patients with glomerulonephropathies indicate that monocyte chemoattractant protein-1 (MCP-1) plays a main role in progression of inflammatory processes in kidney diseases. Monocytes/macrophages are multifunctional cells that may regulate matrix accumulation by producing transforming growth factor beta-1 (TGF-beta-1), which plays an important role in the progression of renal diseases. The present study was undertaken to evaluate the relationships between the immunoexpression of MCP-1, the number of CD68-positive cells, the immunoexpression of TGF-beta-1 and the extent of renal fibrosis as well serum creatinine level in patients with lupus nephritis. Using immunohistochemistry we analyzed the expression of MCP-1, TGF-beta-1 and the number of CD68+ cells in renal biopsy specimens in 17 patients with IV class of lupus nephritis and in 10 normal kidneys. Statistical analysis revealed significant increase in the tubulointerstitial MCP-beta immunostaining in lupus nephritis as compared to normal controls. In lupus nephritis the amount of glomerular and interstitial CD68+ cells was higher than in control group. None of the control sections have evidence of glomerular or tubulointerstitial immunoexpression of TGF-beta-1. In patients with lupus nephritis TGF-beta-1 was detected in the renal tubular epithelial cells and the interstitium, and to a lesser extent within glomeruli. The tubulointerstitial MCP-1 immunoexpression was significantly correlated with monocyte/macrophage interstitial infiltrates, the immunoexpression of TGF-beta-1 in tubuli and interstitium as well as serum creatinine. Moreover, the tubulointerstitial immunoexpression of TGF-beta-1 was significantly positively correlated with renal interstitial cortical volume and serum creatinine in patients with lupus nephritis. In summary, these data suggest that in lupus nephritis MCP-1 may play a role in modulating interstitial inflammatory process and in tubulointerstitial renal damage via TGF-beta-1 pathway.