NLRP3 Inflammasome Participates in Host Response to Neospora caninum Infection.

摘要: Neospora caninum is an intracellular protozoan parasite closely related to Toxoplasma gondii that mainly infects canids as the definitive host and cattle intermediate host, resulting in abortion leading financial losses worldwide. Commercial vaccines or drugs are not available for prevention treatment of bovine neosporosis. Knowledge about hallmarks immune response this infection could form basis important strategies. The innate system first responds invading subsequently initiates appropriate adaptive against parasite. Upon infection, activation pattern-recognition receptors expressed by cells triggers response. Toll-like receptors, NOD-like C-type lectin play key roles recognizing Therefore, we aimed explore role NLRP3 inflammasome during acute period N. infection. In vitro results showed murine bone marrow-derived macrophages activated inflammasome, accompanied release IL-1β IL-18, cleavage caspase-1, induction cell death. K+ efflux induced participated inflammasome. Infection mice deficient NLRP3, ASC, caspase-1/11 resulted decreased production IL-18 reduced IFN-γ serum. Elevated numbers monocytes/macrophages neutrophils were found at initial site, but they failed limit replication. These findings suggest involved stage plays limiting growth, it may enhance Th1 inducing IFN-γ. help devise protocols controlling