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1.  Differentiating Glomerular Inflammation from Fibrosis in A Bone Marrow Chimera for Rat Anti-GBM Glomerulonephritis 
American journal of nephrology  2015;42(1):42-53.
Background
Many types of glomerulonephritis (GN) undergo tandem connected phases: inflammation and fibrosis. Fibrosis in human GNs leads to irreversible end stage disease. This study investigated how these two phases were controlled.
Methods
Using a rat anti-glomerular basement membrane (GBM) GN model, we established bone marrow (BM) chimeras between GN-resistant Lewis (LEW) and GN-susceptible Wistar Kyoto (WKY) rats. Glomerular inflammation and fibrosis were compared between chimeras.
Results
LEW’s BM to WKY (WKYLEW) chimeras with or without co-transfer of host WKY’s T cells were GN-resistant. On the other hand, WKY’s BM to LEW (LEWWKY) chimeras developed glomerular inflammation and albuminuria upon immunization. Quantitative analysis showed that the number and composition of inflammatory cells in glomeruli of immunized LEWWKY chimeras were similar to those in immunized WKY rats at their inflammatory peak. Thus, glomerular inflammation was controlled by BM derived non-T cell populations. However, unlike WKY rats, LEWWKY rats did not develop fibrosis until the end of experiments (84 days) in spite of persistent inflammation and albuminuria.
Conclusion
Inflammation alone was not sufficient to trigger fibrosis, suggesting a critical role of glomerular cells in the fibrotic process. As LEWWKY chimera allows us to separate glomerular inflammation from fibrosis, this model provides a useful tool to study how fibrosis is initiated following inflammation.
doi:10.1159/000438929
PMCID: PMC4651783  PMID: 26337665
Glomerulonephritis; fibrosis; animal models

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