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Who is in control of the stickleback immune system: interactions between Schistocephalus solidus and its specific vertebrate host

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons56903

Scharsack,  Jörn Peter
Department Evolutionary Ecology, Max Planck Institute for Evolutionary Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons56771

Koch,  Kamilla
Department Evolutionary Ecology, Max Planck Institute for Evolutionary Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons56711

Hammerschmidt,  Katrin
Department Evolutionary Ecology, Max Planck Institute for Evolutionary Biology, Max Planck Society;

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Citation

Scharsack, J. P., Koch, K., & Hammerschmidt, K. (2007). Who is in control of the stickleback immune system: interactions between Schistocephalus solidus and its specific vertebrate host. Proceedings of the Royal Society B-Biological Sciences, 274(1629), 3151-3158. doi:10.1098/rspb.2007.1148.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000F-D72D-6
Abstract
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.