TUMOR NECROSIS FACTOR ALPHA LEVELS IN THE RAT BRAIN AND CEREBROSPINAL FLUID AFTER MENINGITIS INDUCED BY STREPTOCOCCUS PNEUMONIAE 

Tatiana Barichello (UNESC); Ivonete dos Santos (UNESC); Geovana Dagostin Savi (UNESC); Anelise Feliciano Florentino (UNESC); Jaqueline da Silva Generoso (UNESC); Clarissa M. Comim (UNESC); Daniela Sachs (UFMG); Mauro M. Teixeira (UFMG); Antonio L. Teixeira (UFMG); João Quevedo (UNESC)

Introduction: Bacterial meningitis due to Streptococcus pneumoniae is associated with a a considerable inflammatory reaction in the meninges, with significant mortality rate of up to 30% and persisting neurologic sequelae including sensory-motor, deficits, seizures, and impairments of learning and memory in up to 50% of the survivors. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process include tumor necrosis factor alpha (TNF-a), interleukin (IL)-1b, IL-6. TNF-a have several effects, including cytotoxicity, antiviral activity, transcription factor activation, and immune response regulation. Objective: Thus, the aim of this study was to verify the levels of the TNF-a after pneumococcal meningitis in male Wistar rats. Methods: All surgical procedures and bacteria administrations were performed under anesthesia consisting of an intraperitoneal administration of ketamine (6.6mg/kg), xylazine (0.3 mg/kg), and acepromazine (0.16 mg/kg). Animals males Wistar rats underwent a magna cistern tap receiving either 10 µL sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration 5x10⁹ cfu/mL. The animals were killed by decapitation 0, 6, 12, 24, 48 and 96 h after induction. The brain was removed and hippocampus, cortex, prefrontal and cerebrospinal fluid were isolated and used for the determination of TNF-a levels. Results: We found an increase in TNF-a levels at six hours after induction of the meningitis in the hippocampus, frontal cortex, and cerebrospinal fluid. There was no alteration in the córtex. Conclusions: Our data suggest that TNF-a can be a putative biomarker for brain damage in the first hours of the pneumococcal meningitis.