Rajakumar Sethu, Bleiss Wilfrid, Hartmann Susanne, Schierack Peter, Marko Anorte, Lucius Richard
Department of Molecular Parasitology, Institute of Biology, Humboldt-University Berlin, Philippstr. 13, 10115 Berlin, Germany.
J Parasitol. 2006 Feb;92(1):41-5. doi: 10.1645/GE-3507.1.
In an attempt to study the occurrence of concomitant immunity in filarial infections, jirds (Meriones unguiculatus) were experimentally infected with Acanthocheilonema viteae, and patent animals were superinfected with a defined dose of A. viteae stage 3 larvae (L3). Infected animals harbored significantly less worms deriving from the superinfection than the control group (P < 0.05, 56.2%, and 63.4% protection), as shown by analysis of female worms 6 wk after superinfection on the basis of their developmental status and their length. This protection was not due to contact with L3 antigens because a significant reduction of worm burdens deriving of a superinfection was also observed after subcutaneous implantation of a single female worm (P < 0.05, 40.2% and 64.9% protection). The induced protective responses target L3 and restrict their migration because an established infection resulted in a reduction of L3 recovery (95.6% and 94.3%, P < 0.001) from tissues of jirds at day 5 after superinfection. Other data show that L3 from a superinfection are trapped within eosinophil-rich granulomas, which is likely to create unfavorable conditions for the worms and to lead to later death. Taken together, established A. viteae-infections partially protect hosts against homologous superinfection by an immune-mediated mechanism and, thus, regulate the population density of the parasites within the host by concomitant immunity.
为了研究丝虫感染中伴随免疫的发生情况,将沙鼠(长爪沙鼠)用魏氏棘唇线虫进行实验性感染,对出现虫血症的动物用确定剂量的第3期幼虫(L3)进行再次感染。如在再次感染6周后根据雌虫的发育状态和长度进行分析所示,感染动物体内源自再次感染的虫体数量显著少于对照组(P<0.05,保护率分别为56.2%和63.4%)。这种保护作用并非由于接触L3抗原,因为在皮下植入单条雌虫后,再次感染导致的虫体负荷也显著降低(P<0.05,保护率分别为40.2%和64.9%)。诱导的保护性反应针对L3并限制其迁移,因为已建立的感染导致再次感染后第5天沙鼠组织中L3回收率降低(95.6%和94.3%,P<0.001)。其他数据表明,再次感染的L3被困在富含嗜酸性粒细胞的肉芽肿内,这可能为虫体创造不利条件并导致其后期死亡。综上所述,已建立的魏氏棘唇线虫感染通过免疫介导机制部分保护宿主免受同源再次感染,从而通过伴随免疫调节宿主体内寄生虫的种群密度。