Ling Li
Jiaotong University School of Medicine, China
Posters & Accepted Abstracts: J Neurol Neurophysiol
The risk of serious sequelae causing by the central nerve system (CNS) infection is 30-60%. Among them, inflammation is one of the critical mechanisms. But how inflammation alters brain function remains unclear. Here, we provide a solid evidence of meningitis caused by brain damage reduced host inflammatory response. Neurotrophic factor family plays an important role in neurons development, differentiation and survival. BDNF expression increased in acute S. pneumonia meningitis, while obviously alleviated after antibiotic treatment. Neonatal meningitis caused long-term BDNF decrease was correlated to adult animalsâ?? behavioral deficits. Exogenous BDNF can increase neuron survival both in the cortex and hippocampus, and reversed brain damage. Meanwhile, it can increase hippocampus neuron stem cells neurogenesis. These findings indicate that BDNF regulatory expression may be parts of host inflammatory response in S. pneumoniae meningitis, and innate immune response could be a double-edged blade. Although the mechanism is still unknown. According to in vivo pneumococcal meningitis experimental models, we investigated BDNF-related signaling effects inflammatory response and hippocampal apoptosis. Before S. pneumoniae intracisternal infection, we pretreatment with exogenous BDNF or TrkB inhibitor k252a and assess BDNF/TrkB-signaling axis activation or inhibition. Administered BDNF in rats reduced clinical impairment, pathological severity, and hippocampal apoptosis Furthermore, BDNF pretreatment suppressed inflammatory factors (TNFα, IL-1β, and IL-6) expression while increased anti-inflammatory factor IL-10. It also increased TrkB expression, activated downstream PI3K/protein kinase B (AKT) signaling, and inhibited MyD88/NF-κBsignaling pathway. These results indicated that exogenous BDNF treatment might be a potentially effective therapeutic strategy for inflammatory brain injury. Here is a 2-year-old boy with acute necrotizing encephalopathy by infection. After timely treatments with high-dose methylprednisolone and, immunoglobulin therapy, multiple vitamins and nerve growth factor. He had the relatively good prognosis and could see neuroregeneration in follow-up brain MRI (Fig 1).
E-mail: liling@xinhuamed,com.cn
