NRTUAs感染对小鼠的组织荷虫量及脾脏细胞因子转录水平的影响

Impacts of NRTUAs infection on the parasite load and the transcriptional levels of splenic cytokines in mice

为进一步研究非增殖型尿嘧啶营养缺陷型弓形虫(NRTUAs)对小鼠的致病性,本研究以NRTUAs和Δku80虫株分别感染小鼠,每日检测各组小鼠的组织荷虫量,并检测感染后1~3d脾脏相关细胞因子的转录水平。结果表明:1)NRTUAs感染的小鼠不能在7d内清除虫体,NRTUAs刺激小鼠脾脏上调IL-12、TNF-α和IL-10的表达,并诱导温和的炎症反应;2)Δku80虫株感染的小鼠在感染后6d内死亡,组织荷虫量平均水平高于NRTUAs感染的小鼠,Δku80虫株刺激小鼠脾脏上调IL-12、TNF-α、IL-1β、IL-6、IFN-γ和IL-10的表达,诱导剧烈的炎症反应而导致小鼠死亡。综上,NRTUAs对小鼠的致病性较低,NRTUAs组织荷虫量平均水平低于Δku80组,诱导机体的炎症反应显著轻于Δku80组,为NRTUAs作为畜禽免疫增强剂的开发提供研究基础。

In order to further explore the pathogenicity of nonreplicating Toxoplasma uracil auxotrophs(NRTUAs)in mice,mice were infected with NRTUAs orΔku80 strain to detect parasite load for each group daily and the transcriptional levels of related splenic cytokines within 1to 3days after parasite infection.The results indicated that:1)NRTUAs were not completely removed from the mice within 7days.NRTUAs stimulated the spleen of mice to upregulate the expression of IL-12,TNF-αand IL-10,which induced a mild inflammatory response.2)While mice infected withΔku80 strain were dead within 6days and the average parasite load was higher than that of NRTUAs infected mice.Δku80 strain stimulated the spleen of mice to up-regulate the expression of IL-12,TNF-α,IL-1β,IL-6,IFN-γand IL-10,which induced severe inflammatory response to cause the death of mice.In summary,the pathogenicity of NRTUAs to mice was low and the average parasite load was less than that ofΔku80 strain infected mice.The inflammatory response of mice stimulated by NRTUAs was lighter than that ofΔku80 strain infected mice.This study laid a theoretical foundation for the application of NRTUAs as immunopotentiator in livestock and poultry breeding.