Acanthamoeba spp. areopportunistic, facultative parasites that can cause a severe potentially blinding keratitis and a fatal encephalitis in humans. Toll-Like Receptors (TLRs) are pattern recognition receptors (PRR) expressed on innate immune cells, including macrophages that are known to participate in the immune response to Acanthamoeba. The aim of our study was to elucidate the role of TLRs on monocytes/macrophages, in the recognition and response to Acanthamoeba castellanii. For this purpose, both human and murine models have been used, combining the advantages of these two different systems. Results demonstrate that the release of pro-inflammatory cytokines by murine macrophages after challenge with Acanthamoeba is MyD88 dependent and TRIF independent. In human monocytes cytokine production stimulated by trophozoites is ablated by blocking TLR4. In contrast, blocking TLR2 ablates cytokine production to molecules released by Acanthamoeba. Taken together our study indicates that TLRs and their associated signaling pathways play important roles in Acanthamoeba infections, in both human and murine systems
Evidence for MyD88-dependent, TRIF-independent activation of Toll-like Receptors by Acanthamoeba castellanii using human and murine systems / A., Cano; F., Henriquez; M., Sanna; J., Alexander; Robert, C. W.; Mattana, Antonella. - (2013). (Intervento presentato al convegno 15th International Meeting on the Biology and Pathogenicity of Free-living Amoebae. tenutosi a Vienna nel 14-19 Luglio 2013).
Evidence for MyD88-dependent, TRIF-independent activation of Toll-like Receptors by Acanthamoeba castellanii using human and murine systems.
MATTANA, Antonella
2013-01-01
Abstract
Acanthamoeba spp. areopportunistic, facultative parasites that can cause a severe potentially blinding keratitis and a fatal encephalitis in humans. Toll-Like Receptors (TLRs) are pattern recognition receptors (PRR) expressed on innate immune cells, including macrophages that are known to participate in the immune response to Acanthamoeba. The aim of our study was to elucidate the role of TLRs on monocytes/macrophages, in the recognition and response to Acanthamoeba castellanii. For this purpose, both human and murine models have been used, combining the advantages of these two different systems. Results demonstrate that the release of pro-inflammatory cytokines by murine macrophages after challenge with Acanthamoeba is MyD88 dependent and TRIF independent. In human monocytes cytokine production stimulated by trophozoites is ablated by blocking TLR4. In contrast, blocking TLR2 ablates cytokine production to molecules released by Acanthamoeba. Taken together our study indicates that TLRs and their associated signaling pathways play important roles in Acanthamoeba infections, in both human and murine systemsI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
