Ohno Tamio, Kai Takuya, Miyasaka Yuki, Maruyama Haruhiko, Ishih Akira, Kino Hideto
Division of Experimental Animals, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Division of Experimental Animals, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Parasitol Int. 2018 Aug;67(4):357-361. doi: 10.1016/j.parint.2018.02.003. Epub 2018 Feb 12.
Hymenolepis diminuta is a parasitic tapeworm of the rat small intestine and is recognized as a useful model for the analysis of cestode-host interactions. In this study, we analyzed factors affecting the biomass of the tapeworm through use of rat strains carrying genetic mutations, namely X-linked severe combined immunodeficiency (xscid; T, B and NK cells deficiency), nude (rnu; T cell deficiency), and mast cell deficient rats. The worm biomass of F344-xscid rats after infection with 5 cysticercoids was much larger than control F344 rats from 3 to 8 weeks. The biomass of F344-rnu rats was also larger than the controls, but was intermediate between F344-xscid and control rats. These observations demonstrated that host immunity can control the maximal tapeworm biomass, i.e., carrying capacity, of the rat small intestine. Both T cell and other immune cells (B and NK cells) have roles in determining the carrying capacity of tapeworms. Total worm biomass and worm numbers in mast cell deficient rats (WsRC-Ws/Ws) were not significantly different from control WsRC-+/+ rats after 3 and 6 weeks of primary infection. Mast cell deficient rats displayed reinfection resistance for worm biomass but not worm expulsion. These findings suggest that the mast cell has a role for controlling the biomass of this tapeworm in reinfection alone, but does not affect the rate of worm expulsion. Overall, our findings indicate that the mast cell is not a major effector cell for the control of the carrying capacity of tapeworms. The identity of the major effector cell remains unknown.
微小膜壳绦虫是大鼠小肠内的一种寄生绦虫，被认为是分析绦虫与宿主相互作用的有用模型。在本研究中，我们通过使用携带基因突变的大鼠品系，即X连锁严重联合免疫缺陷大鼠（xscid；T、B和NK细胞缺陷）、裸鼠（rnu；T细胞缺陷）和肥大细胞缺陷大鼠，分析了影响绦虫生物量的因素。感染5个似囊尾蚴后，F344-xscid大鼠在3至8周时的虫体生物量比对照F344大鼠大得多。F344-rnu大鼠的生物量也比对照大鼠大，但介于F344-xscid大鼠和对照大鼠之间。这些观察结果表明，宿主免疫可以控制大鼠小肠内绦虫的最大生物量，即承载能力。T细胞和其他免疫细胞（B细胞和NK细胞）在决定绦虫的承载能力方面都发挥作用。初次感染3周和6周后，肥大细胞缺陷大鼠（WsRC-Ws/Ws）的总虫体生物量和虫体数量与对照WsRC-+/+大鼠无显著差异。肥大细胞缺陷大鼠对再次感染的虫体生物量表现出抵抗力，但对虫体排出没有抵抗力。这些发现表明，肥大细胞仅在再次感染时对控制这种绦虫的生物量起作用，但不影响虫体排出率。总体而言，我们的研究结果表明，肥大细胞不是控制绦虫承载能力的主要效应细胞。主要效应细胞的身份仍然未知。
