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Gene regulation in Streptococcus pneumoniae - RePub - Erasmus ...

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1.5 x 10 5 vs 5.8 x 10 4 CFU/ml at 12h. This suggests that there might be an <strong>in</strong>itial positive<br />

effect of the psaR-mutation, as the <strong>in</strong>oculum of the wild-type conta<strong>in</strong>ed (more than) twice as<br />

many bacteria than that of the psaR-mutant (1.2 x 10 6 and 4.5 x10 5 and CFU/ml,<br />

respectively).<br />

In contrast, mice <strong>in</strong>fected with the TIGR4 psaR-mutant had lower bacterial loads <strong>in</strong><br />

the lungs compared to mice <strong>in</strong>fected with TIGR4 wild-type, although these differences were<br />

only statistically significant at 24h post-<strong>in</strong>fection (P=0.0401) (Fig. 3B).<br />

The number of bacteria that were able to reach the systemic circulation was not<br />

significantly different between wild-type and ΔpsaR <strong>in</strong> either D39 or TIGR4 (data not<br />

shown), <strong>in</strong>dicat<strong>in</strong>g that PsaR-<strong>regulation</strong> is not required for the transition from the lungs to the<br />

systemic circulation.<br />

Figure 3. Pneumonia model. Bacterial loads <strong>in</strong> lungs and blood of mice <strong>in</strong>fected with (A) D39 wild-type and<br />

D39ΔpsaR, (B) TIGR4 wild-type and TIGR4ΔpsaR. * <strong>in</strong>dicates P < 0.05.<br />

PsaR and pneumococcal virulence<br />

PsaR contributes to survival of pneumococci dur<strong>in</strong>g bacteremia<br />

The most prom<strong>in</strong>ent phenotype of the psaR-mutants was observed <strong>in</strong> the bacteremia<br />

model of <strong>in</strong>fection. D39 wild-type-<strong>in</strong>fected mice had significantly more bacteria <strong>in</strong> the blood<br />

75<br />

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