Iványi B, Krenács T, Petri S
Virchows Arch B Cell Pathol Incl Mol Pathol. 1985;50(1):59-70. doi: 10.1007/BF02889890.
Acute pyelonephritis was induced in rats by temporary unilateral ureteric obstruction and the intravenous injection of Escherichia coli. Animals were sacrificed 48 h after infection and changes in renal cortical tubules due to the presence of bacteria were studied. Bacteria appeared and multiplied in the tubular lumina and proximal tubular epithelial cells endocytosed the microorganisms in large numbers. Coalescence of phagosomes with lysosomes resulted in the surrounding of engulfed bacteria with acid phosphatase. However, the lysosomal apparatus of the cells did not eliminate Escherichia coli since the bacteria multiplied within phagosomes and destroyed the normal cell architecture. The peritubular interstitial inflammatory infiltrate caused ischemia of tubules, enhancing bacterial damage to the proximal tubules. The cytoplasm of the injured tubular cells was sometimes detached from the basement membrane. Cells of the distal tubules and collecting ducts did not show significant endocytosis or bacterial tubular damage.
通过暂时单侧输尿管梗阻和静脉注射大肠杆菌在大鼠中诱发急性肾盂肾炎。感染后48小时处死动物,研究因细菌存在而导致的肾皮质小管变化。细菌出现在小管腔中并繁殖,近端小管上皮细胞大量内吞微生物。吞噬体与溶酶体融合导致被吞噬的细菌被酸性磷酸酶包围。然而,细胞的溶酶体装置并未清除大肠杆菌,因为细菌在吞噬体内繁殖并破坏了正常的细胞结构。肾小管周围间质炎性浸润导致小管缺血,加重细菌对近端小管的损伤。受损肾小管细胞的细胞质有时会与基底膜分离。远端小管和集合管的细胞未显示明显的内吞作用或细菌对小管的损伤。