Figure 2: Disruption of CTR4 induces inflammatory responses and lung damage.

(a) Infected lung tissues from C57BL/6 mice were perfused, dissected and photographed after 14 days of infection (scale bar=0.5 cm). (b) Infected lung tissues (n=9) were weighed, and the data were plotted (mean, s.d.). Statistical analysis was performed using Student’s t-test (***P<0.005 and **P<0.01). (c,d) Infected lung tissues from C57BL/6 mice were stained with haematoxylin and eosin and examined under a × 5 lens (c) (scale bar=100 μm) and a × 10 lens (d) (scale bar=50 μm). Arrows indicate immune cells. (e) Infected lung tissues from c were subjected to TUNEL staining (scale bar=25 μm). Stained cells are indicated with arrows. (f) The number of apoptotic cells of each strain was quantified. Statistical analysis was performed using Student’s t-test. The data are presented as the mean±s.d. Four different microscopy views were selected and stained cells were counted (***P<0.005). (g) Biofilm formation by each strain was assayed and quantified as described previously⁵⁷. Statistical analysis was performed using Student’s t-test. The data are presented as the mean±s.d. (h) Enumeration of Blood CFUs. C57BL/6 mice (n=5) were infected as described in Fig. 1 for 14 and 21 days. Blood samples were collected and plated on SC agar plates for 3 days. Statistical analysis was performed using ANOVA (*P<0.05).