Apoptosis Is Essential for Neutrophil Functional Shutdown and Determines Tissue Damage in Experimental Pneumococcal Meningitis
Figure 1
Transgenic Bcl-2 blocks the resolution of inflammation in pneumococcal meningitis.
Groups of 7 mice (24 h) and 12 mice (72 h) were infected with pneumococci and in the case of 72 h analysis treated with antibiotics starting at 24 h. (A) CSF leucocyte counts were determined in samples obtained by puncture of the cisterna magna by counting in a Fuchs-Rosenthal chamber. Absolute neutrophil counts were calculated on the basis of these numbers and the relative numbers of neutrophils as assessed by Giemsa staining of CSF smears. These numbers were 10,122±5,763 (mean/SD of 6 mice) in wt and 11,471±6,036 in Bcl-2 transgenic mice (not significantly different). (B–F) cytokine levels were determined in brain lysates and are expressed as levels per total protein. (B) Levels of IL-1β, (C) levels of G-CSF; *P<0.05, Bcl-2 transgenic mice compared to wt mice at 72 h. (D) Levels of active TGF-ß in brain homogenates of wt mice (n = 7 (0 h), 7 (24 h), 12 (48 h), 12 (72 h)) and Bcl-2 transgenic mice (n = 7 (24 h) and n = 9 (72 h)), *P<0.05, (wt mice vs. Bcl-2 transgenic mice). (E) Levels of IL-1 receptor antagonist (IL-1ra; *P<0.05, Bcl-2 transgenic mice compared to wt mice at 72 h), (F) levels of IL-6.