IMMUNOLOGY OF PYELONEPHRITIS IN THE PRIMATE MODEL .5. EFFECT OF SUPEROXIDE-DISMUTASE
IMMUNOLOGY OF PYELONEPHRITIS IN THE PRIMATE MODEL .5. EFFECT OF SUPEROXIDE-DISMUTASE
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DOI：
10.1016/s0022-5347(17)53516-8
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发表时间：
1982-01-01
影响因子：
6.6
通讯作者：
BASKIN, G
中科院分区：
文献类型：
--
作者：
ROBERTS, JA;ROTH, JK;BASKIN, G
通过输尿管导管将细菌输注到肾内反流点，在猴子中产生上行性急性肾盂肾炎。这导致显著的炎症反应，肾小管粒细胞和细菌区域的肾小管细胞死亡。给予超氧化物歧化酶，炎症反应降低，肾小管细胞被杀死的数量减少。与吞噬中性粒细胞相邻的肾小管细胞超微结构变化也减少。这表明细菌感染后的肾损伤可能是由于在吞噬作用期间产生并释放超氧化物进入肾小管腔。显然，这是最初的事件，可能会导致肾组织和功能的最终损失称为慢性肾盂肾炎。
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. Superoxide dismutase was given, and 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. Evidently, it is the initial event which may lead to the eventual loss of renal tissue and function called chronic pyelonephritis.