Wei Xiao-li, Ding Jian-bing, Xu Yan, Wen Hao, Lin Ren-yong
Basic Medicine College of Xinjiang Medical University, Urumqi 830054, China.
Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi. 2004 Dec;22(6):361-4.
To observe the change of six cytokines in mice infected with Echinococcus multilocularis as part of the study on immunological mechanism in the infection.
Mice were infected by abdominal inoculation of echinococcus protoscoleces. The change of serum level of the cytokines IL-2, IFN-gamma, TNF-alpha, IL-4, IL-5 and IL-10 was determined by ELISA during the infection which lasted for 260 d.
Compared with uninfected control, the levels of the cytokines all significantly increased in the 260 d. The level of IL-2 reached a peak after 80 d post-infection (p.i.), then decreased quickly after 140 d p.i., High level of TNF-alpha was detected after 40 d, compared to uninfected control, reached a peak at 100 d p.i., and decreased quickly after 140 d. The level of IFN-gamma reached a peak after 80 d p.i., and decreased slowly after 140 d p.i. The levels of IL-4, IL-5 and IL-10 remained lower before 80 d, and increased sharply after 100 days. The levels of IL-4 and IL-10 reached peaks at 100 d p.i., and that of IL-5 at 140 d p.i.
The data suggest that the induction of Th2 antibody-mediated immunity (AMI) with a parallel expansion of Th1 cell-mediated inflammatory (CMI) responses are important mechanism of the host in defending against the metacestodes. Th1 CMI plays an important role at the early stage of infection, and Th2 AMI is important in the later stage of infection.
观察多房棘球绦虫感染小鼠后六种细胞因子的变化,作为该感染免疫机制研究的一部分。
通过腹腔接种棘球绦虫原头节感染小鼠。在持续260天的感染过程中,采用酶联免疫吸附测定法(ELISA)测定细胞因子白细胞介素-2(IL-2)、γ-干扰素(IFN-γ)、肿瘤坏死因子-α(TNF-α)、白细胞介素-4(IL-4)、白细胞介素-5(IL-5)和白细胞介素-10的血清水平变化。
与未感染对照组相比,在260天的感染过程中,所有细胞因子水平均显著升高。IL-2水平在感染后80天达到峰值,然后在感染后140天迅速下降。TNF-α在感染40天后检测到高水平,与未感染对照组相比,在感染后100天达到峰值,并在感染后140天迅速下降。IFN-γ水平在感染后80天达到峰值,并在感染后140天缓慢下降。IL-4、IL-5和IL-10水平在80天前较低,在100天后急剧升高。IL-4和IL-10水平在感染后100天达到峰值,IL-5在感染后140天达到峰值。
数据表明,Th2抗体介导的免疫(AMI)的诱导以及Th1细胞介导的炎症(CMI)反应的平行扩展是宿主抵御幼虫的重要机制。Th1 CMI在感染早期起重要作用,而Th2 AMI在感染后期起重要作用。