B. ABORTUS DOWN MODULATES INFLAMMATION IN MONOCYTES/MACROPHAGES THROUGH MTOR ACTIVATION

AGUSTINA PILAR MELNYCZAJKO,; PESCE VIGLIETTI, AYELÉN IVANA; ARRIOLA BENITEZ, PAULA CONSTANZA; GENTILINI, MARÍA VIRGINIA; LOPEZ MALIZIA, ALVARO; DELPINO M VICTORIA; GIAMBARTALOMEI, GUILLERMO; RODRIGUEZ ANA M

Congreso; LXVIII REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INMUNOLOGÍA (SAI); 2020

Brucellosis, caused by Brucella spp, is a disease with a large inflammatorycomponent. B. abortus has been shown to activatecells of innate immunity, inducing the secretion of pro-inflammatoryfactors. However, B. abortus has different mechanisms whereby itmodulates the immune response, in order to evade it and surviveintracellularly. mTOR (mammalian target of rapamycin) is a proteinkinase that regulates essential signaling pathways, regulating severalcellular functions, such as innate immunity, among others. Theaim of this work was to elucidate whether B. abortus can modulatethe functionality of monocytes and macrophages through the activationof mTOR. B. abortus was capable to activate mTOR (evaluatedby flow cytometry) during the infection of human monocytesand murine macrophages (RAW 264.7). As heat-killed B. abortusrecapitulates the effect, we concluded that bacterial viability is notnecessary to induce mTOR activation. A significant increase in theexpression of TNF-α (p