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Although more and more new potent antibiotics have been used, mortality and neurologic deficits still occur frequently following bacterial meningitis in children. In this article, the expression of brain-derived neurotrophic factor messenger ribonucleic acid (RNA) and its production in the brains of rats were investigated during the course of experimental bacterial meningitis and after treatment with an antibiotic plus dexamethasone. In the brains of Streptococcus pneumoniae-inoculated rats, brain-derived neurotrophic factor (BDNF) messenger RNA was obviously up-regulated after inoculation for 24 hours (P < .01) and then declined but was still greater than that in the brains of control rats after inoculation for 5 days (P < .05). The expression of brain-derived neurotrophic factor in the brains of infected rats treated by antibiotic was dose dependent, down-regulated, and almost undetectable (P < .01) but up-regulated after treatment with an antibiotic plus dexamethasone (P < .01). However, the expression of brain-derived neurotrophic factor messenger RNA did not change in control rats treated with an antibiotic. Brain-derived neurotrophic factor protein showed similar changes, except it declined to normal levels 5 days after inoculation. Brain-derived neurotrophic factor messenger RNA and its production were observed in some infiltrating inflammatory cells in the brain of infected rats. The results of our studies support the hypothesis that brain-derived neurotrophic factor might play a neuroprotective role in brain damage during bacterial meningitis, and the expression of brain-derived neurotrophic factor messenger RNA and its production might be inhibited after treatment with antibiotics. The findings suggest that both eradicating the bacterial pathogen with antibiotics and adjuvant administering of brain-derived neurotrophic factor might be more beneficial to prevent brain damage.

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Bacterial meningitis is still one of the most common causes of acquired profound sensorineural deafness in children despite antibiotic treatment. We investigated the neuroprotective effects of brain-derived neurotrophic factor on hearing function in experimental bacterial meningitis. We implanted stainless steel tubes into both cerebral ventricles of Sprague-Dawley rats aged 21 days. Bacterial meningitis was induced by inoculating a strain of serotype III Streptococcus pneumoniae into the cisterna magna. Six micrograms per day of brain-derived neurotrophic factor (groups 1 and 3) or albumin (groups 2 and 4) was injected into the cerebral ventricles 24 hours after or before infection, respectively, for a duration of 7 days. Additionally, all rats received antibiotic subcutaneous treatment starting 24 hours after infection for 7 days. Brainstem auditory evoked potentials were recorded 24 hours before and 24 hours after infection and after 7 days of treatment with brain-derived neurotrophic factor or placebo and antibiotics, respectively, to determine hearing threshold. Our results showed that the hearing thresholds of animals in each group increased significantly 24 hours after infection compared with the results recorded 24 hours before infection (P < .01). After 7 days of treatment with brain-derived neurotrophic factor, brainstem auditory evoked potential responses recurred in 16 ears when stimulated at 75 dB hearing level in groups 1 and 3. Their hearing thresholds significantly decreased compared with the control group 2 (P < .05) and group 4 (P < .01). However, 13 of 14 ears absent brainstem auditory evoked potential responses could still not be identified at 75 dB hearing level in control groups 2 and 4. The improvement of the hearing thresholds in group 3 (treated before infection) was greater than that of group 1 (treated after infection) (P < .05), but there was no significant difference found between the control groups before and after infection (P > .05). Our study supports the hypothesis that the administration of exogenous brain-derived neurotrophic factor can be effective in preventing or treating hearing loss following bacterial meningitis.

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