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Background  The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacterium  Streptococcus (S.) pneumoniae . CCAAT/enhancer binding protein δ is a transcription factor that has recently been hypothesized to play a detrimental role in outcome of meningitis caused by  S. pneumoniae . Here, we studied the role of C/EBPδ prior to the development of pneumococcal meningitis.    Methods  Wild-type and C/EBPδ-deficient mice (C/EBPδ −/− ) were intraveneously infected with  S. pneumoniae  and sacrificed after 24 or 48 h.  cebp δ expression, bacterial loads, inflammatory response and pathology in the brain were assessed.    Results    S. pneumoniae  induces  cebp δ expression in the brain during blood-borne brain infection. In comparison to wild-type mice, C/EBPδ −/−  animals showed decreased bacterial loads in blood and brain 48 h after inoculation. In the blood compartment, the host inflammatory response was significantly lower upon infection in C/EBPδ −/−  mice as compared to wild-type mice.    Conclusion  C/EBPδ facilitates bacterial dissemination to the brain and enhances the immune response in the blood compartment. Our study suggests that C/EBPδ plays a detrimental role during the initial development of blood-borne brain infection.

Detrimental role for CCAAT/enhancer binding protein δ in blood-borne brain infection