Mechanism of Central Nervous System Dysfunction in Toxoplasma gondii Infection

弓形虫是一种专性胞内寄生虫，可入侵多种脊椎动物宿主细胞。弓形虫的慢性感染建立在中枢神经系统的组织中，在那里寄生虫可能直接或间接调节神经功能。然而，弓形虫引起的神经元紊乱的机制仍不清楚。本研究的目的是阐明弓形虫感染过程中神经元紊乱的分子和细胞机制。本研究利用RNA-seq技术分析弓形虫感染后小鼠脑内宿主基因的表达。因此，上调的基因主要参与宿主免疫反应和细胞激活。相比之下，与寄生虫数量呈负相关的基因被预测与神经功能有关。此外，还建立了小鼠小胶质细胞的原代培养体系，并在小胶质细胞中产生细胞因子和一氧化氮，以对抗弓形虫感染。

Toxoplasma gondii is an obligate intracellular parasite that invades a wide range of vertebrate host cells. Chronic infections with T. gondii become established in the tissues of the central nervous system where the parasites may directly or indirectly modulate neuronal function. However, the mechanisms of T. gondii-induced neuronal disorder remain unclear. The objective of this study is to elucidate the molecular and cellular mechanisms of neuronal disorder during T. gondii infection. In this study, host gene expression in mouse brain following infection with T. gondii was analyzed by RNA-seq. As a result, the up-regulated genes were primarily involved in host immune responses and cell activation. In contrast, genes that had a negative correlation with parasite numbers were predicted to be involved in neurological function. In addition, primary culture system of murine microglia was established, and cytokines and nitric oxide were produced in microglia against T. gondii infection.