P-fimbriae have been found to be a virulence factor in both human and nonhuman primate urinary tract infections caused by Escherichia coli. This is because of bacterial adherence to urothelial cells which is mediated by adherence of fimbriae to a specific glycolipid receptor on the cell membrane of these cells. We purified P-fimbriae for immunization of monkeys. High titers of antifimbrial antibody protected against both acute and chronic pyelonephritis after renal inoculations of P-fimbriate Escherichia coli.

Cranberry juice irreversibly inhibits P-fimbriae. Electron micrographic evidence suggests that cranberry juice acts on the cell wall preventing proper attachment of the fimbrial subunits or as a genetic control preventing the expression of normal fimbrial subunits or both.

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.