| First Author | Valls Serón M | Year | 2015 |
| Journal | J Neuroinflammation | Volume | 12 |
| Pages | 88 | PubMed ID | 25958220 |
| Mgi Jnum | J:319138 | Mgi Id | MGI:6862851 |
| Doi | 10.1186/s12974-015-0309-5 | Citation | Valls Seron M, et al. (2015) CCAAT/enhancer-binding protein delta (C/EBPdelta) aggravates inflammation and bacterial dissemination during pneumococcal meningitis. J Neuroinflammation 12:88 |
| abstractText | BACKGROUND: The prognosis of bacterial meningitis largely depends on the severity of the inflammatory response. The transcription factor CAAT/enhancer-binding protein delta (C/EBPdelta) plays a key role in the regulation of the inflammatory response during bacterial infections. Consequently, we assessed the role of C/EBPdelta during experimental meningitis. METHODS: Wild-type and C/EBPdelta-deficient mice (C/EBPdelta(-/-)) were intracisternally infected with Streptococcus pneumoniae and sacrificed after 6 or 30 h, or followed in a survival study. RESULTS: In comparison to wild-type mice, C/EBPdelta(-/-) mice showed decreased bacterial loads at the primary site of infection and decreased bacterial dissemination to lung and spleen 30 h after inoculation. Expression levels of the inflammatory mediators IL-10 and KC were lower in C/EBPdelta(-/-) brain homogenates, whereas IL-6, TNF-alpha, IL-1beta, and MIP-2 levels were not significantly different between the two genotypes. Moreover, C/EBPdelta(-/-) mice demonstrated an attenuated systemic response as reflected by lower IL-10, IL-6, KC, and MIP-2 plasma levels. No differences in clinical symptoms or in survival were observed between wild-type and C/EBPdelta(-/-) mice. CONCLUSION: C/EBPdelta in the brain drives the inflammatory response and contributes to bacterial dissemination during pneumococcal meningitis. C/EBPdelta does, however, not affect clinical parameters of the disease and does not confer a survival benefit. |
