Included in this respository is all code used for the manuscript and all datafiles. For more information about fibrosis scores in fish, please see manuscript and accompanying video. All analysis were done in R. Please contact Amanda Hund with additional questions (ahund@umn.edu).\u00a0
\nFunding provided by: James S Mcdonnell Foundation
Crossref Funder Registry ID: http://dx.doi.org/10.13039/100000002
Award Number: Postdoctoral Fellowship to Hund
Funding provided by: American Association of Immunologists
Crossref Funder Registry ID: http://dx.doi.org/10.13039/100002570
Award Number: Intersect Postdoctoral Fellowship to Fuess
Funding provided by: University of Connecticut
Crossref Funder Registry ID: http://dx.doi.org/10.13039/100007710
Award Number: Startup funds to Bolnick
Funding provided by: National Institutes of Health
Crossref Funder Registry ID: http://dx.doi.org/10.13039/100000002
Award Number: NIAID Grant 1R01AI123659-01A1
Closely related populations often differ in resistance to a given parasite, as measured by infection success or failure. Yet, the immunological mechanisms of these evolved differences are rarely specified. Does resistance evolve via changes to the host's ability to recognize that an infection exists, actuate an effective immune response, or attenuate that response? We tested whether each of these phases of the host response contributed to threespine sticklebacks' recently evolved resistance to their tapeworm Schistocephalus solidus. While marine stickleback and some susceptible lake fish permit fast-growing tapeworms, other lake populations are resistant and suppress tapeworm growth via a fibrosis response. We subjected lab-raised fish from three populations (susceptible marine 'ancestors', a susceptible lake population, a resistant lake population), to a novel immune challenge using an injection of: 1) a saline control, 2) alum, a generalized pro-inflammatory adjuvant that causes fibrosis, 3) a tapeworm protein extract, or 4) a combination of alum and tapeworm protein). With enough time, all three populations generated a robust fibrosis response to the alum treatments. Yet, only the resistant population exhibited a fibrosis response to the tapeworm protein alone. Thus, these populations differed in their ability to respond to the tapeworm protein but shared an intact fibrosis pathway. The resistant population also initiated fibrosis faster in response to alum, and was able to attenuate fibrosis, unlike the susceptible populations' slow but longer-lasting response to alum. As fibrosis has pathological side-effects that reduce fecundity, the faster recovery by the resistant population may reflect an adaptation to mitigate the costs of immunity. Broadly, our results confirm that parasite detection and immune initiation, activation speed, and immune attenuation simultaneously contribute to the evolution of parasite resistance and adaptations to infection in natural populations.
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