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Title: | Intrinsic renal cells are the major source of interleukin-1beta synthesis in normal and diseased rat kidney. | Authors: | Atkins R.C.;Tesch G.H.;Yang N.;Yu H.;Lan H.Y.;Foti R.;Chadban S.J.;Nikolic-Paterson D.J. | Institution: | (Tesch, Yang, Yu, Lan, Foti, Chadban, Atkins, Nikolic-Paterson) Department of Nephrology, Monash Medical Centre, Clayton, Vic., Australia (Nikolic-Paterson) Department of Nephrology, Monash Medical Centre, Clayton Road, Clayton, Vic. 3168, Australia | Issue Date: | 22-Oct-2012 | Copyright year: | 1997 | Publisher: | Oxford University Press (Great Clarendon Street, Oxford OX2 6DP, United Kingdom) | Place of publication: | United Kingdom | Publication information: | Nephrology Dialysis Transplantation. 12 (6) (pp 1109-1115), 1997. Date of Publication: June 1997. | Abstract: | Background. A number of studies have demonstrated a pathological role for interleukin-1 (IL-1) in experimental models of glomerulonephritis, but the cellular pattern of renal IL-1 production remains poorly characterized. The aim of this study, therefore, was to identify the cell types expressing IL-1 in normal and diseased rat kidney. Methods. Renal IL-1beta expression was examined in normal rats and during a 21-day time course of rat accelerated anti-GBM glomerulonephritis by northern blotting, in situ hybridization and double immunohistochemistry. Results. Interleukin-1beta mRNA expression was readily detectable in normal rat kidney by northern blot analysis and in situ hybridization. Immunohistochemistry staining demonstrated constitutive IL-1beta expression by glomerular endothelial cells and cortical tubular epithelial cells. There was a marked increase in whole kidney IL-1beta mRNA in rat anti-GBM glomerulonephritis. Glomerular IL-1beta immunostaining was upregulated, being expressed by podocytes, mesangial cells and infiltrating macrophages, and was particularly prominent within glomerular crescents. Double staining with the ED1 antibody showed IL-1beta expression in up to 13% of glomerular macrophages, whereas 48% of macrophages within crescents stained for IL-1beta. However, the most marked increase in IL-1beta expression was seen in cortical tubular epithelial cells, particularly in areas of tubular damage. In situ hybridization confirmed that tubular IL-1beta staining was due to local cytokine synthesis rather than protein absorption. Conclusions. This study has identified constitutive IL-1beta expression by glomerular endothelium and tubular epithelial cells in normal rat kidney. In addition, the marked upregulation of IL-1beta expression by intrinsic glomerular cells and tubules in rat anti-GBM disease suggests an important role for these cells in IL-1 dependent crescent formation and tubulointerstitial injury. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1093/ndt/12.6.1109 | PubMed URL: | 9198037 [http://www.ncbi.nlm.nih.gov/pubmed/?term=9198037] | ISSN: | 0931-0509 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/33846 | Type: | Article |
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