The impairment in the NLRP3-induced NO secretion renders astrocytes highly permissive to T. cruzi replication.

摘要: Trypanossoma cruzi (T. cruzi), the causative protozoan of Chagas disease (CD) invades many cell types, including central nervous system (CNS) cells triggering local lesions and neurological impact. Previous work from our group described NLRP3 inflammasomes as effectors for parasite control by macrophages. Recent evidences demonstrate that can be activated in CNS with controversial consequences to infections inflammatory pathologies. However, relative contribution different types remains elucidated. In this article, we an effector response mediated works on microglia but not astrocytes T. infection. Despite ability invade microglia, were clearly more permissive replication. Moreover, absence renders fact, able secrete NLRP3-dependent IL-1β NO cruzi. Importantly, pharmacological inhibition iNOS aminoguanidine resulted a significant increase numbers amastigotes found wild-type NLRP3-/- mice, indicating importance NLRP3-mediated secretion infection these cells. Taken together, findings revealed differentially activates established role platforms glial CNS.