Effects of Toxoplasma gondii infection on the brain
Effects of Toxoplasma gondii infection on the brain
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DOI：
10.1093/schbul/sbm008
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发表时间：
2007-05-01
影响因子：
6.6
通讯作者：
Suzuki, Yasuhiro
中科院分区：
文献类型：
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作者：
Carruthers, Vern B.;Suzuki, Yasuhiro
刚地弓形虫是一种细胞内的原生寄生虫，可以通过三种不同的方式感染人类：吞食组织包囊、吞食卵囊或先天性感染速殖子。在急性期速殖子在各种器官中增殖后，寄生虫优先在脑中形成包囊并建立慢性感染，这是宿主免疫和寄生虫逃避免疫应答之间的平衡。各种脑细胞，包括星形胶质细胞和神经元，都可以被感染。使用非脑细胞的体外研究已经证明了感染对宿主细胞基因表达的深刻影响，包括促进免疫反应的分子和参与信号转导途径的分子，这表明类似的影响可能发生在受感染的脑细胞中。干扰素-γ是控制T.弓形虫在大脑中维持慢性感染的潜伏期。感染还诱导小胶质细胞、星形胶质细胞和神经元产生多种细胞因子，其促进或抑制炎症反应。T.弓形虫、宿主的遗传因素、可能的感染途径和寄生虫启动感染的阶段（速殖子、包囊或卵囊）都有助于建立宿主和寄生虫之间的平衡并影响感染的结果。
Toxoplasma gondii, an intracellular protozoan parasite, can infect humans in 3 different ways: ingestion of tissue cysts, ingestion of oocysts, or congenital infection with tachyzoites. After proliferation of tachyzoites in various organs during the acute stage, the parasite forms cysts preferentially in the brain and establishes a chronic infection, which is a balance between host immunity and the parasite's evasion of the immune response. A variety of brain cells, including astrocytes and neurons, can be infected. In vitro studies using non-brain cells have demonstrated profound effects of the infection on gene expression of host cells, including molecules that promote the immune response and those involved in signal transduction pathways, suggesting that similar effects could occur in infected brain cells. Interferon-gamma is the essential mediator of the immune response to control T. gondii in the brain and to maintain the latency of chronic infection. Infection also induces the production of a variety of cytokines by microglia, astrocytes, and neurons, which promote or suppress inflammatory responses. The strain (genotype) of T. gondii, genetic factors of the host, and probably the route of infection and the stage (tachyzoite, cyst, or oocyst) of the parasite initiating infection all contribute to the establishment of a balance between the host and the parasite and affect the outcome of the infection.