03/15/2024
By Irma Silva

The Kennedy College of Sciences, Department of Biological Sciences, invites you to attend a Ph.D. Dissertation Defense in Applied Biology by Alexandra Collias entitled:"Characterization of stickleback immune modulation by the cestode Schistocephalus solidus: divergent in vitro and in vivo responses."

Candidate: Alexandra Collias
Date: Wednesday, April 3, 2024
Time: 11 a.m. to 1 p.m.
Location: Pulichino Tong Building 130

Advisor: Natalie Steinel, Assist. Professor, Biological Sciences, University of Massachusetts Lowell


Committee members:

  • Peter Gaines, Chair & Professor, Biological Sciences, University of Massachusetts Lowell
  • Rick Hochberg, Assoc. Professor, Biological Sciences, University of Massachusetts Lowell
  • Elia Tait-Wojno, Associate Professor, Immunology, University of Washington

Title: Characterization of stickleback immune modulation by the cestode Schistocephalus solidus: divergent in vitro and in vivo responses.

Brief Abstract: Helminths infect over 1 billion people worldwide, causing pathologies that lead to 9 million disability-adjusted life years (DALY’s) lost in children alone, and disrupting the socioeconomic state, health, and wellbeing of the communities affected. Helminths perpetuate disease directly by damaging host tissues, and indirectly by suppressing their host’s immune response. Mechanisms of immune suppression include directly reducing immune cell populations by initiating apoptosis or restricting their proliferation, indirectly reducing them by inhibiting their activation signals, or by dampening their effector functions. These effects are known to be mediated by soluble products produced by the parasite known as excretory-secretory (ES) products. An opportune model for studying parasite-mediated immune modulation is the threespine stickleback fish (Gasterosteus aculeatus) and its cestode, Schistocephalus solidus. S. solidus infection causes reduced body condition, reproductive success, and disrupted sleeping patterns. S. solidus can reduce the phagocytic capacity of immune cells, decrease the size of splenic aggregates of phagocytic cells known as melanomacrophages (MMCs), and downregulate genes involved in the adaptive immune response, including some responsible for lymphocyte activation and migration. While expression of genes associated with lymphocyte responses have been characterized, the direct presence of these cells in the lymphoid tissues has yet to be observed. Studies on S. solidus-mediated immune modulation have focused on a single lymphoid tissue, the head kidney, but modulation of responses in the stickleback spleen, an important secondary lymphoid tissue, has yet to be examined. To address this gap we assessed the effect of S. solidus on immune phenotypes in vitro and in vivo in the stickleback spleen. We found that exposure to S. solidus ES products maintained stickleback splenocyte viability and increased reactive oxygen species (ROS) production, suggesting that ES products enhance some aspects of splenocyte immunity. In contrast, S. solidus infection significantly reduced the presence of IgM+ B and CD4+ T cells in stickleback splenic tissue, accompanied by a reduction in IgMhigh expressing cells, indicating that in vivo infection with S. solidus modulates adaptive immunity by suppressing lymphocyte responses. We also found significant variation in these responses that was dependent on the parasite’s lake of origin, signifying that some parasites may have evolved diverging strategies of host manipulation. This work furthers our understanding of S. solidus-mediated immunomodulation by centering an important lymphoid tissue in fish, the spleen, and by specifically identifying the downregulation of lymphocytes with infection. We also contribute to the current knowledge of parallel evolution in stickleback populations infected with S. solidus. As a whole, this work presents additional evidence for ES products as immunomodulators and identifies cestode infections as regulators of lymphocyte responses.