Who is in control of the stickleback immune system: interactions between Schistocephalus solidus and its specific vertebrate host
Who is in control of the stickleback immune system: interactions between Schistocephalus solidus and its specific vertebrate host
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DOI：
10.1098/rspb.2007.1148
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发表时间：
2007-12
期刊：
影响因子：
--
通讯作者：
J. Scharsack;Kamilla Koch;K. Hammerschmidt
中科院分区：
文献类型：
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作者：
J. Scharsack;Kamilla Koch;K. Hammerschmidt
苏氏血吸虫是一种常见的三刺刺鱼寄生虫，对宿主的适合性有很大影响。因此，在刺鱼防御机制(如有效的免疫系统)以及克服这些的寄生虫策略上，选择压力应该很大。尽管有迹象表明，鞭虫操纵了其特定第二中间宿主的免疫系统，但目前尚不清楚固链菌与刺鱼免疫系统的特定相互作用的年表。在这里，我们期望刺鱼首先在接触寄生虫后直接启动先天免疫反应，以在早期阶段清除感染，并在最初的滞后阶段之后上调适应性免疫。最有趣的是，我们没有发现任何特定的淋巴细胞介导的免疫反应上调。此外，天然免疫系统的激活模式也与我们的预期不符：单核细胞的增殖遵循波动动力学，这表明寄生虫反复安装新的表面涂层，而不是对宿主产生免疫原性。此外，呼吸爆发活动有可能清除早期的固态链球菌感染，在感染很晚的时候被上调，当时寄生虫太大，无法清除，但准备传播到最终宿主。我们认为先天免疫系统的后期激活干扰了神经内分泌系统，神经内分泌系统调节了减少的捕食回避行为，从而促进了对最终宿主的传播。
The cestode Schistocephalus solidus is a frequent parasite of three-spined sticklebacks and has a large impact on its host's fitness. Selection pressure should therefore be high on stickleback defence mechanisms, like an efficient immune system, and also on parasite strategies to overcome these. Even though there are indications for manipulation of the immune system of its specific second intermediate host by the cestode, nothing is yet known about the chronology of specific interactions of S. solidus with the stickleback immune system. We here expected sticklebacks to first mount an innate immune response directly post-exposure to the parasite to clear the infection at an early stage and after an initial lag phase to upregulate adaptive immunity. Most interestingly, we did not find any upregulation of the specific lymphocyte-mediated immune response. Also, the pattern of activation of the innate immune system did not match our expectations: the proliferation of monocytes followed fluctuating kinetics suggesting that the parasite repeatedly installs a new surface coat not immunogenic to the host. Furthermore, the respiratory burst activity, which has the potential to clear an early S. solidus infection, was upregulated very late during infection, when the parasite was too big to be cleared but ready for transmission to its final host. We here suggest that the late activation of the innate immune system interferes with the neuroendocrine system, which mediates reduced predation avoidance behaviour and so facilitates the transmission to the final host.