Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice
Mice selected on the basis of an acute inflammatory response (AIR) can provide information about the immunopathological mechanisms of glomerulonephritis. We studied the differences between mice selected for a maximal AIR (AIRmax that attract more polymorphonuclear cells to the site of injury) or a m...
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Associação Brasileira de Divulgação Científica
2005-12-01
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Series: | Brazilian Journal of Medical and Biological Research |
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Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2005001200009 |
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author | R.S. Kurihara M. Yokoo W.V. Domingues W.H. Cabrera O.G. Ribeiro O.M. Ibañez D.A. Malheiros R.T. Barros E.B. de Almeida Prado |
author_facet | R.S. Kurihara M. Yokoo W.V. Domingues W.H. Cabrera O.G. Ribeiro O.M. Ibañez D.A. Malheiros R.T. Barros E.B. de Almeida Prado |
author_sort | R.S. Kurihara |
collection | DOAJ |
description | Mice selected on the basis of an acute inflammatory response (AIR) can provide information about the immunopathological mechanisms of glomerulonephritis. We studied the differences between mice selected for a maximal AIR (AIRmax that attract more polymorphonuclear cells to the site of injury) or a minimal AIR (AIRmin that attract more mononuclear cells) in an experimental model of IgA nephropathy in order to investigate the effect of genetic background on glomerular disease progression and the participation of the monocyte chemoattractant protein-1 (MCP-1) chemokine. IgA nephropathy was induced by intraperitoneal ovalbumin injection and bile duct ligation in AIRmax and AIRmin mice. Histological changes, urinary protein/creatinine ratio, serum IgA levels, immunofluorescence for IgA, IgG and complement C3 fraction, immunohistochemistry for macrophages and MCP-1, and MCP-1 levels in macerated kidney were determined. Mesangial IgA deposition was seen only in AIRmin mice, which presented more renal lesions. Increased serum IgA levels (1.5 ± 0.4 vs 0.3 ± 0.1 mg/mL, P < 0.001), high glomerular MCP-1 expression and decreased monocyte/macrophage infiltration in the interstitial area (0.3 ± 0.3 vs 1.1 ± 0.9 macrophages/field, P < 0.05) were detected in AIRmin mice compared to AIRmax mice. No glomerular monocyte/macrophage infiltration was detected in either strain. In spite of the absence of IgA deposition, AIRmax mice presented discrete or absent mesangial proliferation. The study showed that there are differences between mice selected for AIRmax and AIRmin with respect to serum IgA levels, histological damage and MCP-1 chemokine production after ovalbumin injection in combination with bile duct ligation. |
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spelling | doaj.art-f416bfbde2b14d2bbeec8b1706712c792022-12-21T23:45:11ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X1414-431X2005-12-0138121807181510.1590/S0100-879X2005001200009Genetic potential for an acute inflammatory response in IgA glomerulonephritis in miceR.S. KuriharaM. YokooW.V. DominguesW.H. CabreraO.G. RibeiroO.M. IbañezD.A. MalheirosR.T. BarrosE.B. de Almeida PradoMice selected on the basis of an acute inflammatory response (AIR) can provide information about the immunopathological mechanisms of glomerulonephritis. We studied the differences between mice selected for a maximal AIR (AIRmax that attract more polymorphonuclear cells to the site of injury) or a minimal AIR (AIRmin that attract more mononuclear cells) in an experimental model of IgA nephropathy in order to investigate the effect of genetic background on glomerular disease progression and the participation of the monocyte chemoattractant protein-1 (MCP-1) chemokine. IgA nephropathy was induced by intraperitoneal ovalbumin injection and bile duct ligation in AIRmax and AIRmin mice. Histological changes, urinary protein/creatinine ratio, serum IgA levels, immunofluorescence for IgA, IgG and complement C3 fraction, immunohistochemistry for macrophages and MCP-1, and MCP-1 levels in macerated kidney were determined. Mesangial IgA deposition was seen only in AIRmin mice, which presented more renal lesions. Increased serum IgA levels (1.5 ± 0.4 vs 0.3 ± 0.1 mg/mL, P < 0.001), high glomerular MCP-1 expression and decreased monocyte/macrophage infiltration in the interstitial area (0.3 ± 0.3 vs 1.1 ± 0.9 macrophages/field, P < 0.05) were detected in AIRmin mice compared to AIRmax mice. No glomerular monocyte/macrophage infiltration was detected in either strain. In spite of the absence of IgA deposition, AIRmax mice presented discrete or absent mesangial proliferation. The study showed that there are differences between mice selected for AIRmax and AIRmin with respect to serum IgA levels, histological damage and MCP-1 chemokine production after ovalbumin injection in combination with bile duct ligation.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2005001200009Monocyte chemoattractant protein-1IgAGlomerulonephritisAcute inflammatory responseChemokine |
spellingShingle | R.S. Kurihara M. Yokoo W.V. Domingues W.H. Cabrera O.G. Ribeiro O.M. Ibañez D.A. Malheiros R.T. Barros E.B. de Almeida Prado Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice Brazilian Journal of Medical and Biological Research Monocyte chemoattractant protein-1 IgA Glomerulonephritis Acute inflammatory response Chemokine |
title | Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice |
title_full | Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice |
title_fullStr | Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice |
title_full_unstemmed | Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice |
title_short | Genetic potential for an acute inflammatory response in IgA glomerulonephritis in mice |
title_sort | genetic potential for an acute inflammatory response in iga glomerulonephritis in mice |
topic | Monocyte chemoattractant protein-1 IgA Glomerulonephritis Acute inflammatory response Chemokine |
url | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2005001200009 |
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