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Abstract

The interaction of an organism with its environment is a hallmark of life and prerequisite for natural selection. Among the strongest evolutionary processes is the interaction between hosts and parasites that are engaged in a constant arms race of parasite exploitation and host defense. This antagonistic co-evolution is shaped through host and parasite genotypes, their local environmental conditions, and their potential for plastic responses. However, the relative contribution of these effects is often unclear. Here, I aimed to find answers to the questions how and why epidemiological traits vary among populations by using hosts and parasites from geographically distinct and ecologically divergent populations. I used three-spined sticklebacks (Gasterosteus aculeatus) as vertebrate model organisms to study defense mechanisms against helminth parasites. Helminth parasites are of exceptional interest because they can have complex immune modulatory effects on their hosts. This phenomenon is already applied in clinical settings, where helminths, their ova, or their products are used to treat autoimmune or inflammatory disorders (helminth therapy). Nevertheless, many questions on the specificity of the host-helminth interaction have yet to be answered. For instance: Are there differences between host genotypes or parasite species? What are the effects over time? Are effects localized or systemic? Using evolutionary and ecological perspectives, I specifically asked: What are the effects of host and parasite genotypes and their interaction? Does the potential for interaction effects differ with geographical scale? Does immune modulation differ over the time course of infection, and if so, is the temporal component dependent on parasite strain and/or host type? Indeed, my colleagues and I found that different strains of the same cestode species (Schistocephalus solidus) had profoundly different effects on divergent G. aculeatus types. This effect was linked to the co-evolutionary history and ecology of G. aculeatus and S. solidus. My results demonstrate that the infection outcome was largely determined by effects of host and parasite genotypes, while interaction effects were generally weak and only evident over the scale of continents. Gene expression profiles that differed between uninfected fish from different populations mostly converged upon infection. Thus, the parasite-induced phenotypic plasticity transcended host genetic differences. This thesis also reveals that S. solidus immune modulation is time-, host- and parasite strain-dependent. Sticklebacks that assumingly co-evolved with a highly virulent S. solidus strain were more resistant against S. solidus and had a well-orchstrated immune response (potentially diminishing immunopathological side effects) compared to hosts without this co-evolutionary background. Late stages of infection with a highly virulent S. solidus strain had a systemic effect by increasing the susceptibility towards another helminth species (Diplostomum pseudospathaceum). My data present a snapshot in time and space that provides insights into potential (co-) evolutionary backgrounds. Whether the epidemiological traits of Gasterosteus aculeatus and Schistocephalus solidus are indeed shaped through co-evolution is one of the challenges for future investigations. However, by revealing the dominant effect of the parasite and the relative importance of induced plasticity, this thesis advances our understanding about the role of each partner in a host-parasite interaction. My results are of significant importance for the investigation of the premises and consequences of helminth therapy. I propose to incorporate evolutionary and ecological perspectives in future research.