TRAIL limits excessive host immune responses in bacterial meningitis
J. Clin. Invest. Olaf Hoffmann, et al. 117:2004 doi:10.1172/JCI30356 [Go to this article.]

Figure 2
Leukocyte viability and persistence in the CSF are increased in TRAIL^–/– mice. (A) CSF leukocyte counts at specified time points following meningitis induction. Compared with wild-type C57BL/6 mice, TRAIL^–/– mice show delayed influx of leukocytes into the CSF and delayed resolution of inflammation. **P < 0.01, Student’s t test. (B) Relative proportions of leukocyte subpopulations in the CSF of wild-type and TRAIL^–/– mice at 12, 18, and 24 hours after meningitis induction. Granulocytes (Gran) predominate in the early phase of experimental meningitis in wild-type mice while their accumulation is delayed in TRAIL^–/– mice. Mono, monocytes; Ly, lymphocytes. (C) Proportion of nonviable cells of the total CSF leukocyte concentration at 12, 18, and 24 hours after meningitis induction in wild-type mice and TRAIL^–/– mice as identified by AOEB staining (see also Supplemental Figure 1). Prolonged survival of activated CSF leukocytes is observed in TRAIL^–/– mice. P < 0.01 at 18 hours and at 24 hours; Student’s t test. (D) Leukocyte apoptosis in pooled CSF samples from TRAIL^–/– mice at 12 hours after meningitis induction. One representative experiment out of 2 is shown. rTRAIL (100 ng/ml) accelerates leukocyte apoptosis ex vivo. **P < 0.01, log rank test.