Abstract | BACKGROUND: METHODS: Wild-type and C/EBPδ-deficient mice (C/EBPδ-/-) were intraveneously infected with S. pneumoniae and sacrificed after 24 or 48 h. cebpδ expression, bacterial loads, inflammatory response and pathology in the brain were assessed. RESULTS: S. pneumoniae induces cebpδ 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.
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Authors | JanWillem Duitman, Mercedes Valls Serón, JooYeon Engelen-Lee, Matthijs C Brouwer, C Arnold Spek, Diederik van de Beek |
Journal | BMC infectious diseases
(BMC Infect Dis)
Vol. 16
Issue 1
Pg. 670
(Nov 11 2016)
ISSN: 1471-2334 [Electronic] England |
PMID | 27835970
(Publication Type: Journal Article)
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Chemical References |
- Transcription Factors
- CCAAT-Enhancer-Binding Protein-delta
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Topics |
- Animals
- Bacterial Load
- Brain
(microbiology)
- CCAAT-Enhancer-Binding Protein-delta
(metabolism)
- Humans
- Meningitis, Pneumococcal
(metabolism, pathology)
- Mice
- Mice, Knockout
- Streptococcus pneumoniae
- Transcription Factors
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