B. abortus down modulates inflammation through mTOR activation

PAULA CONSTANZA ARRIOLA BENITEZ; DELPINO, MARÍA VICTORIA; AGUSTINA PILAR MELNYCZAJKO; MARÍA VIRGINIA GENTILINI; GIAMBARTOLOMEI, GUILLERMO HERNÁN; AYELÉN IVANA PESCE VIGLIETTI; ÁLVARO LÓPEZ MALIZIA; ANA MARÍA RODRIGUEZ

Congreso; Reunión anual de SOCIEDADES DE BIOCIENCIAS; 2020

Brucellosis, caused by Brucella spp, is a disease with a large inflammatory component. B. abortus has been shown to activate cells of innate immunity, inducing the secretion of pro-inflammatory factors. However, B. abortus has different mechanisms whereby it modulates the immune response, in order to evade it and survive intracellularly. mTOR (mammalian target of rapamycin) is a protein kinase that regulates essential signaling pathways, regulating several cellular functions, such as innate immunity, among others. The aim of this work was to elucidate whether B. abortus can modulate the functionality of monocytes and macrophages through the activation of mTOR. B. abortus was capable to activate mTOR (evaluated by flow cytometry) during the infection of human monocytes and murine macrophages (RAW 264.7). As heat-killed B. abortus recapitulates the effect, we concluded that bacterial viability is not necessary to induce mTOR activation. A significant increase in the expression of TNF-α (p