Evaluation of the brain-derived neurotrophic factor, nerve growth factor and memory in adult rats survivors of the neonatal meningitis by Streptococcus agalactiae.

Streptococcus agalactiae (GBS) is a major cause of severe morbidity and mortality in neonates and young infants, causing sepsis, pneumonia and meningitis. The survivors from this meningitis can suffer serious long-term neurological consequences, such as, seizures, hearing loss, learning and memory impairments. Neurotrophins, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) control the neuronal cell death during the brain development and play an important role in neuronal differentiation, survival and growth of neurons. Neonate Wistar rats, received either 10µL of sterile saline as a placebo or an equivalent volume of GBS suspension at a concentration of 1×10(6)cfu/mL. Sixty days after induction of meningitis, the animals underwent behavioral tests, after were killed and the hippocampus and cortex were retired for analyze of the BDNF and NGF levels. In the open-field demonstrated no difference in motor, exploratory activity and habituation memory between the groups. The step-down inhibitory avoidance, when we evaluated the long-term memory at 24h after training session, we found that the meningitis group had a decrease in aversive memory when compared with the long-term memory test of the sham group. BDNF levels decreased in hippocampus and cortex; however the NGF levels decreased only in hippocampus. These findings suggest that the meningitis model could be a good research tool for the study of the biological mechanisms involved in the behavioral alterations secondary to GBS meningitis.

Brain-blood barrier breakdown and pro-inflammatory mediators in neonate rats submitted meningitis by Streptococcus pneumoniae.

Neonatal meningitis is an illness characterized by inflammation of the meninges and occurring within the birth and the first 28 days of life. Invasive infection by Streptococcus pneumoniae, meningitis and sepsis, in neonate is associated with prolonged rupture of membranes; maternal colonization/illness, prematurity, high mortality and 50% of cases have some form of disability. For this purpose, we measured brain levels of TNF-α, IL-1ß, IL-6, IL-10, CINC-1, oxidative damage, enzymatic defense activity and the blood-brain barrier (BBB) integrity in neonatal Wistar rats submitted to pneumococcal meningitis. The cytokines increased prior to the BBB breakdown and this breakdown occurred in the hippocampus at 18 h and in the cortex at 12h after pneumococcal meningitis induction. The time-dependent association between the complex interactions among cytokines, chemokine may be responsible for the BBB breakdown and neonatal pneumococcal severity.