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      Immunogold Labelling of Cytokines in Glomeruli in Children with Various Renal Diseases

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          Precise localization of cytokines such as transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), interleukin (IL)-1 and IL-6 was observed in glomeruli using immunogold electron microscopy in 21 children with various types of renal diseases. The distribution pattern of these cytokines, as well as immunoglobulins, C3c and fibrinogen (Fg), was essentially confined to the electron-dense deposits (EDDs) regardless of their location. Frequency of positive labelling of each cytokine was different among various types of renal disorder, that is, TGF-β was found mainly in lupus nephritis (LN), membranous nephropathy and IgA nephropathy, TNF-α in LN, and IL-1 in Henoch-Schönlein purpura nephritis. IL-6 was detected only in 1 case of LN. TNF-α was also found in the cytoplasm of glomerular epithelial cells. Furthermore, in order to evaluate the relation of cytokines to mesangial expansion, extracellular matrix components such as type IV collagen, laminin and fibronectin were stained. The result was that there was no significant correlation between the signal intensity or distribution pattern of cytokines and that of extracellular matrix components. These findings indicate that these cytokines could be associated with the formation of EDDs together with immunoglobulins, C3c and Fg. The involvement of each cytokine in renal pathophysiology might also depend upon the type of renal disease. They also raise the possibility that the glomerular epithelial cells might produce or absorb TNF-α. However, these results did not show significant correlation between cytokine involvement and mesangial expansion.

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          Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1.

          Glomerulonephritis is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli, impaired filtration and proteinuria. In its progressive form, the disease destroys kidney function leading to uraemia and death, unless dialysis therapy or kidney transplantation is available. The pathogenesis of glomerulonephritis is incompletely understood, but the eliciting factor is thought often to be an immunological injury to mesangial and/or other resident cells in the glomeruli. We have used an animal model of acute mesangial proliferative glomerulonephritis to show that this disease is associated with increased production and activity of transforming growth factor beta 1 (TGF-beta 1), an inducer of extracellular matrix production. Here we report that administration of anti-TGF-beta 1 at the time of induction of the glomerular disease suppresses the increased production of extracellular matrix and dramatically attenuates histological manifestations of the disease. These results provide direct evidence for a causal role of TGF-beta 1 in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.
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            Transforming growth factor-β1 induces extracellular matrix formation in glomerulonephritis


              Author and article information

              S. Karger AG
              October 1999
              22 September 1999
              : 83
              : 2
              : 132-138
              aDepartment of Pediatrics, Nara Medical University, Kashihara City, and bPediatric Clinic, Nara Prefectural Nara Hospital, Nara City, Nara, Japan
              45490 Nephron 1999;83:132–138
              © 1999 S. Karger AG, Basel

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              Page count
              Figures: 3, Tables: 2, References: 30, Pages: 7
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/45490
              Original Paper


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