Fig. 6.

cbpJ and cbpL are downregulated in the presence of plasma, and do not affect pneumococcal survival in mouse blood. a Haematoxylin and eosin staining of infected mouse lung tissue collected 24 h after intranasal infection with 5 × 10⁷ CFU of S. pneumoniae TIGR4 WT, ΔcbpL, or ΔcbpJ strains. Scale bars, 200 µm (upper panels), 50 µm (middle panels) and 20 µm (lower panels). b Growth of pneumococcal strains in the presence of human neutrophils. Bacterial cells were incubated with neutrophils for 1, 2 and 3 h at 37 °C and 5% CO₂, then serially diluted and plated on THY blood agar. The number of CFUs was determined following incubation. Growth index was calculated by dividing the CFU after incubation by the CFU of the original inoculum. Data are presented as the mean of six samples with standard error. c Mouse sepsis model. Mice were intravenously infected with 2 × 10⁶ CFU of S. pneumoniae TIGR4 WT, ΔcbpL or ΔcbpJ, and survival was monitored for 14 days. Differences between infected mouse groups were analysed with the log-rank test. d Growth of pneumococcal strains in mouse blood. Bacterial cells were incubated in blood for 1, 2 and 3 h at 37 °C and 5% CO₂. Data are presented as the mean of six samples with standard error. e Fold changes in transcript levels of cbpL and cbpJ in TIGR4 WT S. pneumoniae cells in the presence or absence of human plasma. The 16 S rRNA gene was used as an internal standard. Data were pooled and normalised from three independent experiments, each performed in triplicate. Differences between groups were analysed with the ordinary one-way ANOVA with Tukey’s multiple comparisons test (b, d, e)