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A Fast and Reliable Pipeline for Bacterial Transcriptome Analysis Case study: Serine-dependent Gene Regulation in Streptococcus pneumoniae
Published on: April 25, 2015
Dynamic changes of TrkB gene expression in Streptococcus pneumoniae meningitis after treatment with antibiotics and
Ling Li1, Quan-Xiang Shui, Zheng-Yan Zhao
1Department of Pediatric Neurology, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. lingli12@live.cn
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.
Insights
TrkB signaling may protect the brain in Streptococcus pneumoniae meningitis, but antibiotic treatment might weaken this effect. Targeting TrkB receptors could prevent neurological damage in children.
Area of Science:
- Neuroscience
- Infectious Diseases
- Pharmacology
Background:
- Neurological sequelae of Streptococcus pneumoniae meningitis remain a challenge despite advances in antibiotics.
- Brain-derived neurotrophic factor (BDNF) receptor TrkB mRNA expression is linked to these neurological outcomes.
Purpose of the Study:
- To investigate the role of TrkB mRNA expression in a rat model of Streptococcus pneumoniae meningitis.
- To evaluate the impact of antibiotic and dexamethasone treatment on TrkB mRNA levels.
Main Methods:
- A rat model of Streptococcus pneumoniae meningitis was established.
- Rats were treated with antibiotics or antibiotics plus dexamethasone.
- In situ hybridization was used to detect TrkB gene expression in brain tissue.
Main Results:
- TrkB mRNA was upregulated in infected rat brains within 24 hours.
- Antibiotic treatment led to a dose-dependent downregulation of TrkB mRNA.
- Dexamethasone combined with antibiotics maintained TrkB mRNA upregulation; expression was also noted in inflammatory cells.
Conclusions:
- TrkB signaling pathways likely play a neuroprotective role in Streptococcus pneumoniae meningitis.
- Antibiotic therapy may diminish the protective role of TrkB.
- Targeting TrkB receptors presents a potential strategy to prevent neurological sequelae.
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