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首页> 外文期刊>Vaccine >Immunization with heat-killed Toxoplasma gondii stimulates an early IFN-gamma response and induces protection against virulent murine malaria
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Immunization with heat-killed Toxoplasma gondii stimulates an early IFN-gamma response and induces protection against virulent murine malaria

机译：用热杀死的弓形虫免疫可刺激早期的IFN-γ反应并诱导针对鼠源性疟疾的保护作用

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摘要

BALB/c mice were protected by immunization with heat-killed Toxoplasma gondii tachyzoites against infection with Plasmodium yoelii 17XL, which causes cerebral malaria and death in mice by day 7-8 pi. Immunization resulted in a significant reductionin parasitaemia at the peak period of infection. Protection induced by heat-killed T. gondii was associated with a marked increase in natural killer cell number and interferon (IFN)-gamma messenger RNA expression early in the infection. The level of IFN-gamma or tumour necrosis factor (TNF)-alpha diminished in T. gondii-treated mice as the infection progressed. The diminished response of IFN-gamma or TNF-alpha was associated with a marked increase in expression of interleukin 10. Pretreatment of mice with live T. gondii induced a poor level of protection compared with heat-killed parasites. Mice that received P. yoelii infection alone had an elevated IFN-gamma response in the late stage of infection. Development of cerebral malaria in untreated mice was accompanied by an increased production of TNF-alpha and nitric oxide, the proinflammatory mediators. The results suggest that nonspecific immunization with T. gondii leads to restoration of an early IFN-gamma response in P. yoelii-infected mice and inthe establishment of an immunoregulatory mechanism that effectively antagonizes the disease-promoting effects of proinflammatory cytokines in the late phase of infection.
机译：通过用热灭活的弓形虫速殖子免疫接种BALB / c小鼠，使其免受约氏疟原虫17XL的感染，这会在感染后第7-8天引起小鼠的脑疟疾和死亡。免疫在感染高峰期导致寄生虫血症显着减少。由热杀死的弓形虫诱导的保护作用与感染初期自然杀伤细胞数量和干扰素（IFN）-γ信使RNA表达的显着增加有关。随着感染的进行，刚地弓形虫治疗的小鼠体内的IFN-γ或肿瘤坏死因子（TNF）-α水平降低。 IFN-γ或TNF-α的应答减弱与白介素10的表达显着增加有关。与热杀死的寄生虫相比，用刚地弓形虫进行的小鼠预处理诱导的保护水平较差。单独接受约氏疟原虫感染的小鼠在感染后期具有升高的IFN-γ反应。未经治疗的小鼠脑部疟疾的发展伴随着促炎性介质TNF-α和一氧化氮的产生增加。结果表明，用弓形虫进行的非特异性免疫可导致约耶尔疟原虫感染的小鼠恢复早期的IFN-γ反应，并建立起有效调节促炎细胞因子在疾病晚期的促病作用的免疫调节机制。感染。

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