(465) Schistocephalus solidus suppresses melanomacrophages, IgM+, and CD4+ cells but not IL-17 expression in threespine stickleback (Gasterosteus aculeatus)

Introduction/Rationale: Immunoregulation is critical for maintaining an organism's health, as excessive or deficient immune responses can lead to pathology. Research on humans and other mammals has shown that parasites can affect immune regulation by manipulating their hosts’ immune responses in their favor by suppressing lymphocyte cell survival, activation and/or differentiation. The extent and mechanisms by which parasites modulate fish immunity remains vastly understudied. To address this gap in knowledge, we utilized an emerging immunoparasitological model system: the parasitic tapeworm Schistocephalus solidus, and its host, the threespine stickleback (Gasterosteus aculeatus) fish.

Methods: We evaluated the presence of melanomacrophage centers (MMCs), lymphocytes (IgM and CD4) and pro-inflammatory cytokine Interleukin-17 (IL-17) expression in the spleen of infected and uninfected stickleback. We hypothesized that S. solidus would downregulate stickleback immune response, causing a reduction in splenic MMCs, lymphocytes, and IL-17+ cells.

Results: The results of these studies showed a significant reduction in the size of MMC aggregates and the frequency of IgM+ and CD4+ cells, suggesting S. solidus is capable of suppressing both myeloid and lymphocyte development, recruitment, and/or activation. However, we found no significant difference in IL-17 expression between infected and uninfected fish.

Conclusion: These preliminary findings indicate S. solidus has broad effects on host immunity, expanding our limited knowledge of the mechanisms underlying parasite-mediated immunomodulation in fish and laying the foundation for future work studying local vs systematic immune responses.