Autophagy induction by TLR2 ligands regulate neuroinflammatory response

ARROYO DANIELA S; GAVIGLIO EMILIA A; PERALTA RAMOS JAVIER M; BUSSI CLAUDIO; 1GARCÍA-KELLER CONSTANZA; 1CANCELA LILIANAM; RODRIGUEZ GALÁN MARÍA C E IRIBARREN PABLO

Los Cocos

Congreso; LXI Reunión anual de la Sociedad Argentina de Inmunología; 2013

Sociedad Argentina de Inmunología

Microglial cells (MC) are phagocytes in the central nervous system (CNS) that become activated in pathological conditions, resulting in microgliosis, manifested by increased cell numbers and inflammation in the affected regions. Thus, controlling microgliosis is important to prevent pathological damage to the brain. We previously observed that activation of MC with peptidoglycan (PGN) from S. aureus and another synthetic Toll-like receptor 2 (TLR2) ligand (Pam3CSK4) results in the induction of autophagy. Due to the potential of TLR2 to act as up-regulator of autophagy in MC, here, we examined if the activation of this receptor can regulate the production of pro-inflammatory molecules in brain MC by inducing autophagy. We observed that PGN or Pam3CSK4 induced nitric oxide production in MC, was significantly reduced in the presence of autophagy inhibitors (3-MA or LY294002)(p