Bille J, Glauser M P
J Infect Dis. 1982 Aug;146(2):220-6. doi: 10.1093/infdis/146.2.220.
Previous experiments in rats have suggested that renal scarring after acute, obstructive pyelonephritis due to Escherichia coli results from parenchymal damage due to acute inflammation and suppuration. To assess the role of acute infiltration by polymorphonuclear leukocytes (PMNLs) in the pathogenesis of chronic pyelonephritis (CPN), rats were either treated with colchicine to depress leukocyte motility or rendered neutropenic with a single dose of cyclophosphamide. Colchicine given during acute pyelonephritis reduced kidney inflammation and protected against CPN two months later. Similarly, neutropenia reduced acute inflammation and protected against chronic parenchymal destruction and scarring. Protection against renal scarring in both colchicine-treated and neutropenic rats occurred despite higher renal bacterial counts during acute pyelonephritis. These experiments provide further evidence that CPN (renal scarring) results from kidney damage that occurs during early acute obstructive pyelonephritis. This damage appears to result from infiltration of the kidney by PMNLs rather than direct damage from bacterial infection.
以往在大鼠身上进行的实验表明,大肠杆菌引起的急性梗阻性肾盂肾炎后的肾瘢痕形成是由急性炎症和化脓导致的实质损伤所致。为了评估多形核白细胞(PMNLs)的急性浸润在慢性肾盂肾炎(CPN)发病机制中的作用,对大鼠进行了如下处理:要么用秋水仙碱治疗以抑制白细胞运动,要么用单剂量环磷酰胺使其中性粒细胞减少。在急性肾盂肾炎期间给予秋水仙碱可减轻肾脏炎症,并在两个月后预防CPN。同样,中性粒细胞减少可减轻急性炎症,并预防慢性实质破坏和瘢痕形成。尽管在急性肾盂肾炎期间两组大鼠的肾脏细菌计数较高,但秋水仙碱治疗组和中性粒细胞减少组大鼠的肾脏瘢痕形成均得到了预防。这些实验进一步证明,CPN(肾瘢痕形成)是由早期急性梗阻性肾盂肾炎期间发生的肾脏损伤引起的。这种损伤似乎是由PMNLs浸润肾脏所致,而非细菌感染的直接损伤。