Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensorymotor deficits, seizures, and impairments of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response. Proinflammatory mediators released in the process include tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, and all of which have been shown to contribute to the development of brain injury in bacterial meningitis. The animals underwent a magna cistern tap receiving either 10muL sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration 5x10(9)cfu/mL. Ten days after induction we evaluated depressive-like behavior by using the forced swimming test and verified the levels of the TNF-alpha, IL-1beta, IL-6 and CINC-1 in the brain of rats induced to pneumococcal meningitis. In the forced swimming test we observed a significant increase in the immobility time in the meningitis group compared to the sham group (p<0.05). The TNFlevels were found increased in the prefrontal cortex (p<0.05, F=4.921), but not hippocampus. The IL-6, CINC-1 and IL-1beta levels presented no alteration in both prefrontal cortex and hippocampus 10 days after meningitis induction by S. pneumoniae. 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 pneumococcal meningitis.
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