Waalwijk C, MacLaren D M, de Graaff J
Infect Immun. 1983 Oct;42(1):245-9. doi: 10.1128/iai.42.1.245-249.1983.
The role of hemolysin in the nephropathogenicity of Escherichia coli was studied in a hematogenous pyelonephritis model in mice. The nephropathogenicity of a nonhemolytic, avirulent E. coli strain was increased by simultaneous injection with its hemolytic, nephropathogenic parent. This helper mechanism could be attributed to hemolysin, since the simultaneous injection of partially purified hemolysin gave a similar enhancement of nephropathogenicity. Intraperitoneal injection of hemoglobin or iron sulfate before intravenous challenge with this avirulent strain also led to increased virulence. The nephropathogenicity-enhancing effect of hemolysin is therefore supposed to depend on increasing the level of available iron in the host. Under conditions of plentiful iron, hemolysin production was repressed, as shown by in vitro growth experiments in the presence of exogenous iron. These results suggest that the production of hemolysin is regulated by feedback inhibition.
在小鼠血源性肾盂肾炎模型中研究了溶血素在大肠杆菌致肾病性中的作用。通过与其溶血、致肾病的亲本同时注射,非溶血、无毒的大肠杆菌菌株的致肾病性增强。这种辅助机制可归因于溶血素,因为同时注射部分纯化的溶血素可产生类似的致肾病性增强作用。在用这种无毒菌株进行静脉攻击之前腹腔注射血红蛋白或硫酸铁也会导致毒力增加。因此,推测溶血素的致肾病性增强作用取决于增加宿主中可利用铁的水平。如在外源铁存在下的体外生长实验所示,在铁充足的条件下,溶血素的产生受到抑制。这些结果表明溶血素的产生受反馈抑制调节。