Requirements for leukocyte adhesion molecules in nephrotoxic nephritis.

Authors: Mulligan, MS  Johnson, KJ  Todd RF, 3RD  Issekutz, TB  Miyasaka, M  Tamatani, T  Smith, CW  Anderson, DC  Ward, PA 
Citation: Mulligan MS, etal., J Clin Invest. 1993 Feb;91(2):577-87.
Pubmed: (View Article at PubMed) PMID:7679412
DOI: Full-text: DOI:10.1172/JCI116237

Requirements for leukocyte adhesion molecules as well as cytokines have been determined in the rat model of acute nephrotoxic nephritis. Proteinuria (at 24 h) and neutrophil accumulation in renal glomeruli (at 6 h) have been used as the endpoints. For full accumulation in glomeruli of neutrophils as well as full development of proteinuria, requirements have been demonstrated for TNF alpha, (but not IL-1), CD11b (but not CD11a), very late arising-4 (CD49d/CD29), and intercellular adhesion molecule-1 but not endothelial leukocyte adhesion molecule-1 (E-selectin). By immunohistochemical approaches, infusion of antibody to glomerular basement membrane induced glomerular upregulation of intercellular adhesion molecule-1, endothelial leukocyte adhesion molecule-1, and vascular adhesion molecule-1. Treatment of rats with anti-TNF alpha or soluble recombinant human TNF receptor-1 blocked this expression. Renal arterial infusion of TNF alpha induced glomerular expression of all three endothelial adhesion molecules, but infusion of IL-1 beta did not. These data suggest that, in neutrophil and complement-dependent anti-glomerular basement membrane-induced acute nephritis in rats, there are selective requirements for cytokines, beta 1 and beta 2 integrins, and endothelial adhesion molecules. These requirements contrast with those found in other vascular beds in which complement and neutrophil-induced vascular injury has been induced by deposition of immune complexes.

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CRRD ID: 9698425
Created: 2015-02-13
Species: All species
Last Modified: 2015-02-13
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.