Patrick Skelly
Tufts University, MA·Microbiology & Immunology
Schistosomes are parasitic flatworms that cause a chronic, debilitating disease affecting more than 200 million people in over 70 countries. They live for years in the bloodstream of their hosts.
- Fields
Microbiology & Immunology
Biology
Biochemistry
- Topics
schistosomes
Schistosoma mansoni
schistosomiasis
- Grants
- 1 known grant, through Dec 2028
What they work on
- Test the roles of the surface ectoenzymes SmNPP5 and SmATPDase in controlling host hemostasis, the platelet and clotting response, both in vitro and in vivo.
- Determine whether the surface enzymes SmAP and NACE generate adenosine and nicotinamide, nutrients that schistosomes may need for survival and growth.
- Test whether a calpain, a protein-cutting enzyme on the worm surface, impedes coagulation, promotes clot breakdown (thrombolysis) and blocks local thrombus formation in vivo.
- Identify tegumental proteins critical to parasite survival as candidate targets for future drug screens or vaccine trials.
More about the research
Blood should be a hostile place for them, because the host's hemostatic systems (platelets and blood clotting) normally react to foreign objects. Yet the worms seem to provoke little damaging response. This project tests the idea that proteins on the worm's outer surface, called the tegument, explain how they survive. These proteins were identified in the project's previous funding cycle.
Why it matters
Schistosomiasis is a major and widespread human disease. Finding the surface proteins schistosomes rely on to avoid blood clots and gather nutrients could reveal new targets for drugs that kill the worms, or for vaccines. The goal is to disable the parasites and cure infection. Understanding how a parasite controls clotting could also inform broader work on regulating blood coagulation.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Yohei Hisada
University of North Carolina at Chapel Hill, NC·Medicine & Clinical Research
Test whether podoplanin on leukemia blast cells drives platelet loss in acute promyelocytic leukemia by activating platelets through their CLEC-2 receptor, using xenograft and allograft mouse models that reproduce patient clotting abnormalities.
Congqing Wu
University of Kentucky, KY·Medicine & Clinical Research
Determine how NINJ1 in myeloid immune cells such as macrophages contributes to thrombosis. NINJ1 is the protein that actively ruptures the cell membrane during pyroptosis, an inflammatory form of cell death.
The school
Tufts University: 19 labs on PI Pages, $278M a year on research, 144 research doctorates a year.
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