Urinary Tract Infection, Reserch of Infection Mechanism and Its Applicatin

对大肠埃希氏菌和粘质沙雷氏菌菌毛进行了基因克隆，并探讨了黏附物和菌毛结构对实验性肾盂肾炎的影响。大肠埃希氏菌和粘质沙雷氏菌黏附素刺激肾盂肾炎后瘢痕形成，提示ms黏附素刺激感染部位的多核白细胞（PMNs）， PMNs释放活性氧导致肾组织周围组织损伤。超氧化物清除剂如CV3611、埃布selen、类固醇和乌司他丁可抑制ms -毛状菌感染后的肾瘢痕形成。这些清除剂在抗菌剂组合中有效。肾髓质的pmn功能由于高渗透压而受到抑制。抑制PMNs的机制被认为是ATP在Na处的耗尽或在尿素处的直接失活。氧氟沙星和氟罗沙星是新型喹诺酮类抗菌剂，即使在高渗状态下也能增强pmn功能，提示这些药物治疗肾盂肾炎更有效。

Gene cloning of bacterial pili of Eschrichia coli or Serratia marcescens was performed, and effect of structure of adhesine and bacterial pili on the experimental pyelonephritis was investigated. The adhesine on the MS-piliated bacteria of Eschrichia coli and Serratia marcescens stringly stimulated scar formation following pyelonephritis, suggesting that the MS-adhesin stimulated polymorhonuclearleukocytes (PMNs) in the infected site, and PMNs released active oxygen speceis resulting tissue injury arround renal tissue. Renal scarring following infection with MS-piliated bacteria was suppressed by scavengers of superoxide such as CV3611, Ebselen, Steroid and ulinastatin. These scavengers were effective at the combination of antimicrobial agents.PMN-function was suppressed in the renal medulla due to hyperosmolality. The mechanism of suppression of PMNs were thought to be ATP exhausion at Na or direct inactivation at urea. Ofloxacin and fleroxacin, new quinolone antimicrobials, enhanced PMN-function even in hyperosmotic condition, suggesting that these agents were more effective in the treatment of pyelonephritis.