In vivo function of hemolysin in the nephropathogenicity of Escherichia coli.
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.
D000818:Animals; D004926:Escherichia coli / Q000472:pathogenicity*; D005290:Ferric Compounds / Q000494:pharmacology; D006454:Hemoglobins / Q000494:pharmacology; D006460:Hemolysin Proteins / Q000096:biosynthesis / Q000502:physiology*; D007501:Iron / Q000494:pharmacology; D007668:Kidney / Q000382:microbiology*; D051379:Mice; D014774:Virulence
D005290:Ferric Compounds; D006454:Hemoglobins; D006460:Hemolysin Proteins; C024823:ferric sulfate; D007501:Iron