Figure 2: P2R antagonism has no effect on the disease course of PM.

Mice were treated with suramin (given either by the intraperitoneal or the intracisternal route; 20 mg/kg body weight or brain weight, respectively; n = 11 for each group), BBG (applied intraperitoneally; 50 mg/kg body weight; n = 11), or vehicle (untreated infected mice; n = 11). In an additional experimental group, mice were injected intracisternally with water (vehicle) 2 hours prior to infection. Pneumococcal meningitis was induced by intracisternal injection of S. pneumoniae (strain D39). Sixteen hours later, animals were evaluated. (a) The number of white blood cells (WBC) in the CSF was comparable between mice that received P2R antagonists and those that were injected with vehicle. (b) The meningitis-induced rise in intracranial pressure (ICP) was also not altered by treatment with P2R antagonists. (c,d) There were also no between-group differences in the clinical status and in the reduction of body weight. (e,f) Moreover, pneumococcal outgrowth in the brain (as determined by cerebellar titres) and blood was not affected by pre-treatment with P2R antagonists. Data are given as means ± SD. *P < 0.05, compared to infected animals, using ANOVA and Student-Newman-Keuls post-hoc test.