Lesões teciduais e ativação microglial no sistema nervoso central provocados pelo bacillus calmette-guérin

Abstract

Introduction: About a third part third population is infected by the etiological agent of tuberculosis (TB), approximately 1.6 million deaths in 2005. The tuberculous meningitis is one of the most severe forms of the central nervous system (CNS) involvement by TB affecting children, especially, with death rates around 50%. Despite the severity of the clinical presentation, the molecular and cellular mechanisms involved in the pathogenesis of TB commitment in the CNS are still poorly understood. Purpose: To develop a murine model to elucidate the pathophysiology of TB in the CNS and understanding of the molecular events in the production of injury, thus generating more targeted therapies and better therapeutic result. Materials and Methods: We used swiss mice were divided into two experiments. In experiment I was standardized position of the cannula into the lateral ventricle of the CNS, with the aid of stereotactic coordinates in the second experiment was standardized bacterial charge to be injected into the lateral ventricle. After, there was surgery for intracardiac infusion create brain protection, blades series assembly with sections of the brains, which were submitted to staining by Ziehl-Neelsen, Nissl and hematoxylin-eosin. Results and Discussion: The stereotactic coordinates selected for use in the implementation of the cannula into the lateral ventricle are: 0.25 mm posterior to the bregma, 0.5 mm lateral-lateral and 2 mm dorsoventral from bone cap. Tuberculomas found scattered throughout the CNS only in the animals who received a dose of 105 cfu/μL. Conclusion: BCG intracerebroventricular injection causes the formation of tubers that can be characterized by histochemical methods.