BACKGROUND: Although more and more new potent antibiotics have been used, the incidence of neurological sequelae of Streptococcus pneumoniae meningitis has not improved in children over the last decade. The expression of TrkB mRNA, a receptor of brain-derived neurotrophic factor, is associated with the incidence of neurological sequelae of Streptococcus pneumoniae meningitis. METHODS: Rats of 3 weeks old were used to construct a model of Streptococcus pneumoniae meningitis and served as normal controls. They were administered with antibiotics or antibiotics plus dexamethasone, respectively. The expression of the TrkB gene was detected in the brain by in situ hybridization. RESULTS: In the brains of Streptococcus pneumoniae inoculated rats, TrkB mRNA was significantly up-regulated after inoculation for 24 hours, and then down-regulated in a dose-dependent manner after treatment with antibiotics. This up-regulation was seen after treatment with antibiotics plus dexamethasone. TrkB mRNA expression was also observed in some infiltrating inflammatory cells. CONCLUSIONS: The results of the study support the hypothesis that TrkB signal transduction pathways might play an important role in Streptococcus pneumoniae meningitis, probably by protecting the brain from damage. The role of TrkB might be weakened after the treatment with antibiotics. Our findings suggest that targeting TrkB receptors might be a rational strategy for prevention of neurological sequelae caused by Streptococcus pneumoniae meningitis.
BACKGROUND: Although more and more new potent antibiotics have been used, the incidence of neurological sequelae of Streptococcus pneumoniae meningitis has not improved in children over the last decade. The expression of TrkB mRNA, a receptor of brain-derived neurotrophic factor, is associated with the incidence of neurological sequelae of Streptococcus pneumoniae meningitis. METHODS:Rats of 3 weeks old were used to construct a model of Streptococcus pneumoniae meningitis and served as normal controls. They were administered with antibiotics or antibiotics plus dexamethasone, respectively. The expression of the TrkB gene was detected in the brain by in situ hybridization. RESULTS: In the brains of Streptococcus pneumoniae inoculated rats, TrkB mRNA was significantly up-regulated after inoculation for 24 hours, and then down-regulated in a dose-dependent manner after treatment with antibiotics. This up-regulation was seen after treatment with antibiotics plus dexamethasone. TrkB mRNA expression was also observed in some infiltrating inflammatory cells. CONCLUSIONS: The results of the study support the hypothesis that TrkB signal transduction pathways might play an important role in Streptococcus pneumoniae meningitis, probably by protecting the brain from damage. The role of TrkB might be weakened after the treatment with antibiotics. Our findings suggest that targeting TrkB receptors might be a rational strategy for prevention of neurological sequelae caused by Streptococcus pneumoniae meningitis.
Authors: S Chiaramello; G Dalmasso; L Bezin; D Marcel; F Jourdan; P Peretto; A Fasolo; S De Marchis Journal: Eur J Neurosci Date: 2007-09-20 Impact factor: 3.386
Authors: Magda S Jonczyk; Michelle Simon; Saumya Kumar; Vitor E Fernandes; Nicolas Sylvius; Ann-Marie Mallon; Paul Denny; Peter W Andrew Journal: PLoS One Date: 2014-03-03 Impact factor: 3.240