A study from the University of Minnesota details how som

image: A sensitive threespine stickleback fish is pictured alongside three tapeworms in its abdominal cavity. Resistant fish are able to kill tapeworms or limit their growth with scar tissue like fibrosis. The Threespine Stickleback has become a model for evolutionary study because its marine ancestors colonized the freshwater lakes of Vancouver Island about 11,000 years ago.
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Credit: Amanda Hund, University of Minnesota.

They thrive everywhere, from bustling cities to remote rainforests, even in our own backyards. Ubiquitous and shameless mooches, parasites depend on other organisms for their survival.

The impact of parasites on their host varies greatly, ranging from minor irritation to death. Even among host populations that are closely related, the response to parasite infection can differ significantly. Often populations are classified as “resistant” or “susceptible” to a parasite. However, this simplified framework does not tell the whole story.

In a recent study published in Evolution Letters, a team of researchers led by Amanda Hund, a postdoctoral researcher at the University of Minnesota’s College of Biological Sciences, details how parasite resistance occurs in hosts.

To understand how related hosts respond differently to parasitic infection, researchers closely monitored threespine sticklebacks that live in isolated lakes on Canada’s west coast.

“Mature tapeworms can make it difficult for fish to swim or reproduce. It can even manipulate the behavior of the fish to increase the chances of it being eaten by a bird, where the tapeworm is breeding,” says Hund.

The interaction between a host and a parasite can be broken down into several different steps. Understanding where populations differ in these stages shows scientists where evolution is occurring and often determines whether the population is resistant or susceptible to the parasite. Researchers have found that the ability to detect a parasite and quickly trigger an immune response is the most important factor in determining whether the host can resist the parasite or limit its growth. “Applying this approach to more hosts and parasites will allow us to better understand why parasite resistance varies and how it evolves,” Hund says.

The findings could have other implications for human conditions that generate scar tissue similar to the mesh of tissue that resistant fish use to trap the parasite. Hund collaborator Daniel Bolnick, a professor at the University of Connecticut, is continuing to work on this system to better understand its link to human diseases such as cystic fibrosis and liver fibrosis.

“We found naturally evolutionary genetic variation in how quickly fish initiate and recover from a self-destructive immune response. This same harmful immune response exists in humans, so findings in fish have the potential to teach us how our own bodies might recover from damaging conditions more quickly,” Bolnick says.

Funding and support for this work was provided by a James S. McDonnell Foundation Postdoctoral Fellowship (to AKH), ​​an American Association of Immunologists Intersect Postdoctoral Fellowship (to LEF), the University of Connecticut (starting at DIB) and National Institutes of Health NIAID grant 1R01AI123659-01A1 (at DIB).

About the College of Biological Sciences
The College of Biological Sciences at the University of Minnesota is one of two colleges in the United States dedicated to the biological sciences with undergraduate and graduate programs that span the spectrum of life, from molecules to ecosystems. Learn more at cbs.umn.edu.

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