GIAMBARTOLOMEI Guillermo Hernan
congresos y reuniones científicas
Brucella abortus-activated microglia induces neuronal death through cell to cell contact- and nitric oxide-dependet mechanism.
RODRÍGUEZ A. M., MIRAGLIA M. C., DELPINO M. V., GIAMBARTOLOMEI G.
Congreso; LXIII Reunión Anual de la Sociedad Argentina de Inmunología; 2015
Central nervous system invasion by bacteria of the genus Brucellaresults in an inflammatory disorder called neurobrucellosis. B. abortusinfects microglia, eliciting the activation of this cells and the production ofpro-inflammatory mediators. Previously, we demonstrated that B. abortus-ativatedmicroglia induced neuronal death. The aim of this study was to determine the putativemechanism involved in this phenomenon. Primarycultures of murine neurons were cultured alone or co-cultured with microgliafrom primary cultures infected or not with B. abortus. The viability ofneurons after culture was determined by fluorescent microscopy. The role of nitric oxide was evaluated by using aminoguanidine, a selective inhibitor ofiNOS. As expected, B. abortus-infectedmicroglia induced neuronal death (p<0,005).Yet, in the presence of the aminoguanidine neuronal viability doesn?t differ fromnon-infected microglia (p>0.05). To testwhether direct microglial?neuronal interaction was required for the executionof neuronal death, we added microglia to neuronal cultures either directly orphysically separated from neurons on transwell membrane inserts. In this case, weobserved that when the cells were separated by the transwell neuron viabilitywas the same than non-infected microglia in contact with neurons (p>0.05). Thus,B. abortus-activated microglia kills neurons by cell contact through anNO-depended mechanism. These results describe part of the mechanisms whereby B.abortus could induce neuronal death in neurobrucellosis.