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作 者:吴升伟[1] 胡国顺[2] 王正蓉[2] 包怀恩[2]
机构地区:[1]贵州省疾病预防控制中心,贵阳550004 [2]贵阳医学院寄生虫教研室,贵阳550004
出 处:《中国人兽共患病学报》2015年第1期49-52,63,共5页Chinese Journal of Zoonoses
摘 要:目的了解弓形虫PRU株感染小鼠后脑内局部细胞因子对脑组织的免疫病理作用。方法 51只ICR小鼠分为感染组(33只)和对照组(18只),感染组经腹腔注射弓形虫PRU株10个包囊/鼠,对照组腹腔注射同等量的PBS。于感染后第5d、10d、15d、20d、30d和90d,剖杀感染组小鼠5只和对照组小鼠3只,取脑组织,部分作病理切片;部分提取其RNA,检测IFN-γ、IL-4、IL-6和TNF-αmRNA;部分获取脑组织上清液,用ELISA法测定上述细胞因子。结果相对于正常对照组,感染小鼠脑组织中IFN-γ于感染后第5d开始升高,第10d时下降达到最低,之后开始上升;TNF-α在感染第10d或15d时明显降低,接着上升并于第30d时达到高峰;IL-6在感染第5d时开始升高,感染第10d时降至最低,之后缓慢上升,并于第30d后达到高峰;IL-4未见明显变化。结论弓形虫PRU感染ICR小鼠的过程中,脑组织中IFN-γ、IL-6和TNF-α细胞因子在感染第10d或15d的低表达有利于弓形虫逃避宿主的免疫杀伤作用,导致速殖子在脑组织中存活;同时细胞因子的分泌不平衡,导致小鼠脑组织中出现弓形虫包囊与病理变化共存的隐性感染状态。To learn the brain immunopathogenesis in mice infected with Toxoplasma gondii PRU strain with the cytokines in the tissue,51 mice were grouped into the infected and the control.Thirty-three ICR mice were infected intraperitoneally with cysts,and 10 cysts in each,18 mice were injected with PBS as control.Five mice from the infected and three from the control were sacrificed under anesthesia on 5d,10 d,15d,20 d,30d,and 90dpost-infection(p.i.),and the brain tissues were collected for hematoxylin-eosin(HE)staining and RNA extraction followed by examination of IFN-γ,IL-4,IL-6,and TNF-αwith real-time PCR.The rest of the tissues were subjected to ELISA for the cytokines detection.Comparing with the control,IFN-γin the infected mice began to rise on 5d,decreased to the lowest on 10 d,and then began to raise again p.i.TNF-αbegan to decrease obviously from 10 dto 15dp.i,and reached its highest level on 30 dp.i.IL-6increased on 5dp.i,and then decreased to the lowest on 10 dp.i,then rose slightly and reached the highest on 30 dp.i.No remarkable alteration of IL-4was noted.ICR mice infected with T.gondii PRU strain presented an obviously down-regulated expression of IFN-γ,IL-6and TNF-αfrom 10 dto 15dp.i,which might help the parasites survive from the host immune challenge.Additionally,the timing phase of cytokines expression may be responsible for the cyst formation and latent T.gondii infection.
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