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Immunology of pyelonephritis in the primate model. V. Effect of superoxide dismutase
Abstract:
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.
Insights
Superoxide dismutase reduced inflammation and kidney cell death in monkeys with acute pyelonephritis. This suggests superoxide release during bacterial infection contributes to kidney damage.
Area of Science:
- Nephrology
- Microbiology
- Immunology
Background:
- Ascending acute pyelonephritis is a severe kidney infection.
- Bacterial infections trigger inflammatory responses in the kidneys.
- Superoxide may play a role in kidney damage during infection.
Purpose of the Study:
- To investigate the role of superoxide in acute pyelonephritis-induced kidney damage.
- To evaluate the therapeutic potential of superoxide dismutase in pyelonephritis.
Main Methods:
- Acute pyelonephritis was induced in monkeys via bacterial infusion and ureteral catheterization.
- Superoxide dismutase was administered to assess its effects on inflammation and cell death.
- Renal tissue was examined for inflammatory markers and ultrastructural changes.
Main Results:
- Bacterial pyelonephritis caused significant renal inflammation and tubular cell death.
- Superoxide dismutase administration decreased the inflammatory response and reduced tubular cell mortality.
- Ultrastructural damage was diminished in tubular cells near phagocytosing neutrophils.
Conclusions:
- Superoxide production and release into the tubular lumen during phagocytosis contribute to renal damage in bacterial pyelonephritis.
- Superoxide dismutase may offer a protective effect against kidney injury in pyelonephritis.
- This mechanism is implicated as an initial event leading to chronic pyelonephritis and renal function loss.