title: Regulation of brain-derived neurotrophic factor (BDNF) expression following antibiotic treatment of experimental bacterial meningitis.
abstract: 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.
authors.affiliation: Department of Neurology, Affiliated Children's Hospital, School of Medicine, Zhejiang University, Hangzhou, China. hxyd_zjdx@sohu.com
authors.forename: Ling
authors.initials: L
authors.lastname: Li
authors.forename: Quan-Xiang
authors.initials: QX
authors.lastname: Shui
authors.forename: Zheng-Yan
authors.initials: ZY
authors.lastname: Zhao
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects / Q000473:pathology; D001925:Brain Damage, Chronic / Q000473:pathology; D019208:Brain-Derived Neurotrophic Factor / Q000037:antagonists & inhibitors / Q000235:genetics*; D002443:Ceftriaxone / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D015870:Gene Expression / Q000187:drug effects*; D007279:Injections, Subcutaneous; D008586:Meningitis, Pneumococcal / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000900:Anti-Bacterial Agents; D000893:Anti-Inflammatory Agents; D019208:Brain-Derived Neurotrophic Factor; D012333:RNA, Messenger; D002443:Ceftriaxone; D003907:Dexamethasone