BRUCELLA ABORTUS- ACTIVATED MICROGLIA INDUCES NEURONAL DEATH THROUGH CELL TO CELL CONTACT-, NITRIC OXIDE-DEPENDET MECHANISM

ANA M. RODRÍGUEZ; MARIA CRUZ MIRAGLIA; MARIA VICTORIA DELPINO; GUILLERMO GIAMBARTOLOMEI

Buenos Aires

Congreso; SAI-FAIC; 2015

SAI

Central nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. B. abortus infects microglia, eliciting the activation of this cells and the production of pro-inflammatory mediators. Previously, we demonstrated that B. abortus-ativated microglia induced neuronal death. The aim of this study was to determine the putative mechanisms involved in this phenomenon. Primary cultures of murine neurons were cultured alone or co-cultured with microglia from primary cultures infected or not with B. abortus. The viability of neurons after culture was determined by fluorescent microscopy. The role of nitric oxide was evaluated by using aminoguanidine, a selective inhibitor of iNOS. As expected, B. abortus-infected microglia induced neuronal death (p0.05). To test whether direct microglial?neuronal interaction was required for the execution of neuronal death, we added microglia to neuronal cultures either directly or physically separated from neurons on transwell membrane inserts. In this case, we observed that when the cells were separated by the transwell neuron viability was the same than non-infected microglia in contact with neurons (p>0.05). Thus, B. abortus-activated microglia kills neurons by cell contact through an NO-depended mechanism. These results describe part of the mechanisms whereby B. abortus could induce neuronal death in neurobrucellosis.