Immunology of pyelonephritis in the primate model. V. Effect of superoxide dismutase.
Ascending acute pyelonephritis was produced in monkeys by infusion of bacteria through a ureteral catheter to the point of intrarenal reflux. This led to a significant inflammatory response with death of renal tubular cells in the area of the tubular granulocytes and bacteria. We gave superoxide dismutase, and found that the inflammatory response was decreased and fewer tubular cells were killed. Ultrastructural change was also decreased in tubular cells adjoining phagocytosing neutrophils. This suggests that renal damage following a bacterial infection may be due to the production and release of superoxide into the tubular lumen during phagocytosis. We believe that it is the initial event which may lead to the eventual loss of renal tissue and function called chronic pyelonephritis.
D000818:Animals; D002460:Cell Line; D002470:Cell Survival; D002908:Chronic Disease; D004927:Escherichia coli Infections / Q000276:immunology; D005260:Female; D066298:In Vitro Techniques; D007958:Leukocyte Count; D008252:Macaca fascicularis; D008854:Microscopy, Electron; D009504:Neutrophils / Q000276:immunology; D010587:Phagocytosis; D011704:Pyelonephritis / Q000276:immunology*; D013482:Superoxide Dismutase / Q000494:pharmacology*; D013997:Time Factors
D013482:Superoxide Dismutase