Salmonella Minnesota Re 595 lipid A induced nephritis.
Injection of heat killed bacteria into kidney parenchyma results in pathologic lesions similar to chronic pyelonephritis while immunosuppression reverses this phenomenon. These observations and the propensity of lipid A to bind to cell membranes suggest that the lipid component of bacterial lipopolysaccharide antigens may be important in the pathogenesis of kidney tubule cell death. The right kidneys of syngeneic Fischer 344 rats were repeatedly injected with glycolipid prepared from Salmonella minnesota Re 595 cell walls. As a control, the contralateral kidney was injected with normal saline. The inflammatory response observed in the glycolipid injected kidney was significantly greater (p less than 0.005) than the response detected in the contralateral saline injected control kidney. Electron microscopy of kidney tubule cells incubated with peroxidase conjugated glycolipid demonstrated glycolipid bound to the kidney tubule cell plasma membranes. These studies suggest that individual antigenic components can induce kidney lesions and tubule cell death similar to that seen in chronic pyelonephritis.
D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology*; D001665:Binding Sites; D002462:Cell Membrane / Q000378:metabolism; D002470:Cell Survival; D002473:Cell Wall; D005260:Female; D006017:Glycolipids / Q000276:immunology; D007684:Kidney Tubules / Q000276:immunology / Q000473:pathology; D008050:Lipid A / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D011704:Pyelonephritis / Q000276:immunology* / Q000473:pathology; D051381:Rats; D011916:Rats, Inbred F344; D012475:Salmonella / Q000276:immunology*
D000942:Antigens, Bacterial; D006017:Glycolipids; D008050:Lipid A; D008070:Lipopolysaccharides