Human neuronal cells SH-SY5Y as an in vitro model to study Neospora caninum infection and innate immune modulation.

N. caninum actively modulates neuronal innate immunity via TLR7 suppression, potentially facilitating persistent CNS infections in cattle.

This study investigated Neospora caninum infection and innate immune modulation using human neuroblastoma SH-SY5Y cells as an in vitro model for central nervous system (CNS) neurotropic infections. N. caninum is a protozoan parasite responsible for significant economic losses in cattle due to abortion and is known to establish persistent CNS infections. The researchers demonstrated that N. caninum successfully established productive infections in SH-SY5Y cells, with confirmed parasite invasion, intracellular replication, and subsequent host cell lysis. The study characterized time-dependent modulation of innate immune components, focusing on Toll-like receptor 7 (TLR7) and the cathelicidin antimicrobial peptide gene (CAMP). At 24 hours post-infection, TLR7 expression was downregulated while CAMP expression was upregulated, suggesting the parasite may actively suppress innate immune recognition while the host mounts an antimicrobial response. The TLR7 signaling pathway was further characterized by increased MyD88 expression and decreased IRF7 expression, indicating selective modulation of downstream signaling cascades. These findings suggest N. caninum employs immune evasion strategies within neuronal cells by dampening TLR7-mediated antiviral and antiparasitic responses while potentially exploiting alternative pathways. The SH-SY5Y cell line proved to be a viable model for studying neosporosis-related CNS pathology. Understanding these neuronal immune mechanisms may contribute to future therapeutic targets aimed at controlling persistent N. caninum infections in cattle and preventing associated reproductive losses.

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