Type 1 fimbriate strains of Escherichia coli initiate renal parenchymal scarring.

The renal scarring which characterizes chronic pyelonephritis is initiated by bacterial infection and is independent on the activation of an inflammatory response. Although the presence of polymorphonuclear leukocytes (PMN) is essential for initiating the scarring process, the bacterial structures responsible for their activation have not been investigated. In an animal model of chronic pyelonephritis the surface area of the renal scars produced by Type 1 fimbriate escherichia coli (E. coli) was significantly greater than that of those produced by P fimbriate and non-fimbriate strains (P less than 0.01). The activation of human PMN by the same Type 1 fimbriate organisms resulted in a significant release of lysosomal neutral protease activity (P less than 0.001) and activation of the respiratory burst (P less than 0.01). The neutral protease release in response to P fimbriate and non-fimbriate organisms was not significantly increased. The extent of renal scarring also correlated with the release of neutral protease activity (P less than 0.02) and with the degree of activation of the respiratory burst (P less than 0.05). These results demonstrate that the ability of E. coli strains to cause renal scars may be related to their capacity to express Type 1 fimbria, which may be a causative factor in the in vivo activation of the inflammatory response.