Neospora caninum poses as a considerable threat to animal health and generates significant economic impact in livestock production worldwide. Here, we have investigated the mechanism that underlies the participation of the inflammasome complex and Reactive Oxygen Species (ROS) in the regulation of immune responses during N. caninum infection. For that purpose, we used in vitro (bone marrow derived macrophages) and in vivo mouse models of infection. Our results show that NLRP3 and NLRC4 receptors, alongside with ASC and Caspase-1, are required for proper activation of the inflammasome during N. caninum infection. As expected, the engagement of these pathways is crucial for IL-1α, IL-1β, and IL-18 production, as well as the induction of pyroptosis. Our results also show that N. caninum induces ROS production dependent of the inflammasome assembly, which in its turn also depends on MyD88/NF-κB-induced ROS to maintain its activation and, ultimately, lead to restriction of parasite replication.

中文翻译：

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活性氧物种和炎性体之间的相互作用对于限制犬新孢子虫复制至关重要。

犬新孢子虫对动物健康构成相当大的威胁，并对全球畜牧生产产生重大经济影响。在这里，我们研究了炎性体复合物和活性氧 (ROS) 参与调节犬新孢子虫感染期间免疫反应的机制。为此，我们使用了体外（骨髓来源的巨噬细胞）和体内小鼠感染模型。我们的结果表明 NLRP3 和 NLRC4 受体，以及 ASC 和 Caspase-1，是犬新孢子虫感染期间炎性体适当激活所必需的。正如预期的那样，这些途径的参与对于 IL-1α、IL-1β 和 IL-18 的产生以及细胞焦亡的诱导至关重要。我们的结果还表明，犬新孢子虫依赖炎性体组装诱导 ROS 产生，