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. 2019 Jul 29;15(7):e1007987. doi: 10.1371/journal.ppat.1007987

Fig 3. Lack of ComDE and/or AliB results in an attenuated inflammatory response to pneumococcal infection of the CSF.

Fig 3

Pneumococcal meningitis was induced by intracisternal injection of wild type S. pneumoniae D39 (n = 13) or its isogenic ComDE-deficient, AliB-deficient- or AliB-ComDE-double-deficient mutants (each mutant n = 8). Eighteen hours later, CSF white blood cell (WBC) counts (A), IL-1β (B), and CXCL2 (C) levels were determined. (A) Mice infected with the single or double mutants showed significant decreases in CSF pleocytosis, as compared to D39 infected mice. (B) CSF IL-1β concentrations were quite similar in all mice, irrespective of whether mice were infected with D39 or its isogenic mutants. (C) Conversely, mice infected with mutant strains had lower CSF CXCL2 concentrations than those infected with D39, albeit only the difference between mice infected with the double-deficient mutant and the wild-type strain reached statistical significance. In negative controls (mice injected i.c. with PBS instead of S. pneumoniae; n = 8), CSF leukocyte counts were 284 ± 188 cells/μl, whereas IL-1β and CXCL2 levels were below the detection limit. Data are given as means ± SD. * P < 0.05, compared to mice infected with the D39 strain, using One-Way ANOVA and Tukey post-hoc test.