A three-year, $532,935 grant from the National Institutes of Health will place undergraduate students at Worcester Polytechnic Institute at the center of an effort to unravel one of the most dangerous complications of severe infection: the abnormal, life-threatening blood clotting that can accompany sepsis. The award, issued through the NIH’s Academic Research Enhancement Award program, was secured by Solomon Mensah, an assistant professor in WPI’s Department of Biomedical Engineering, whose laboratory studies how the inner lining of blood vessels behaves under inflammatory stress. Rather than concentrating the work in the hands of a small team of graduate researchers, the grant is explicitly designed to open the laboratory door to undergraduates, giving them sustained, hands-on experience with the molecular machinery that governs vascular health while advancing a research question with direct clinical consequences.
Sepsis is the body’s extreme and dysregulated response to infection, a systemic event that floods the circulation with inflammatory signals and can push organs toward failure. Among its most insidious effects is damage to the endothelial cells, the thin layer of cells that lines every blood vessel and normally maintains a smooth, anticoagulant surface. When inflammation injures this lining, the vessel wall can flip from a protective state to a pro-clotting one. In some patients, this shift contributes to the formation of clots that obstruct small vessels, choking off blood supply to tissues and organs. Clots driven by sepsis-associated inflammation can, in severe cases, contribute to stroke and other vascular events, making it urgent to understand precisely how infection translates into thrombosis at the molecular level.
Mensah’s team will focus on a structure that has attracted growing attention in vascular biology: the glycocalyx, a delicate, gel-like coating that decorates the surface of healthy endothelial cells. Composed of membrane-bound proteins, sugar chains, and associated molecules, the glycocalyx acts as both a physical and biochemical buffer between the blood and the vessel wall. It helps repel circulating cells, moderates the passage of molecules, and presents a non-thrombogenic face to the bloodstream. During systemic infection, inflammatory mediators and enzymes can strip away or degrade this protective layer, exposing the underlying cell surface and altering the way the vessel interacts with blood components. A central aim of the WPI project is to define the molecular mechanisms responsible for this degradation, work that could reveal exactly how sepsis dismantles one of the vasculature’s key defenses.
The second major thread of the project concerns a protein with a pivotal role in normal hemostasis: von Willebrand factor. In healthy vessels, von Willebrand factor is tethered to the endothelial surface, anchored by components of the glycocalyx and associated binding partners that the Mensah laboratory intends to identify. Under inflammatory conditions, the protein detaches from the vessel wall and enters the circulating blood, where it can act as a recruitment platform for platelets, the small cellular fragments that aggregate to form clots. By charting which molecular tethers normally hold von Willebrand factor in place, and what happens to those anchors during infection, the researchers hope to explain how a system built to stop bleeding is subverted into one that promotes vessel-blocking clots.
The third objective is perhaps the most clinically ambitious: determining whether a damaged glycocalyx barrier can be rescued. If the protective coating can be restored or stabilized in the wake of sepsis-induced injury, the finding could point toward entirely new treatment strategies aimed not at dissolving clots after they form, but at preventing the vessel lining from becoming pro-thrombotic in the first place. Such an approach would represent a meaningful shift in thinking about sepsis care, where current interventions focus on controlling infection and supporting failing organs. Mensah and his student researchers will test whether the degradation process can be interrupted or reversed, a step the team describes as potentially paving the way for future sepsis therapies.
The project draws on Mensah’s broader research program, which examines the role of the glycocalyx in heart and lung disease. His work sits at the intersection of vascular biology and biomedical engineering, and his career reflects an unusually broad portfolio. He is a fellow of the American Heart Association and has previously devoted effort to the development of low-cost medical devices intended to expand healthcare access in low- and middle-income countries. That combination of fundamental mechanistic inquiry and practical, globally minded engineering shapes the ethos of the new grant, which treats rigorous laboratory training and meaningful mentorship as inseparable from the scientific questions themselves.
Mensah’s commitment to mentoring is rooted in his own trajectory. As a first-generation student from Africa, he credits mentors with guiding him through the preparation for doctoral studies and shaping his development as a researcher. He has said that he wants to pay those experiences forward by mentoring students and offering them genuine opportunities to conduct research. The NIH award operationalizes that commitment on a concrete scale: Mensah expects it will provide research opportunities to twelve WPI undergraduates. Those students will participate in course-related research projects, individual research work, and Major Qualifying Projects, the capstone experiences that every WPI undergraduate must complete in order to graduate. Embedding the sepsis research within this required structure means the work will reach students across the curriculum rather than remaining confined to a single laboratory cohort.
The Academic Research Enhancement Award program under which the grant is issued has a specific mission: supporting research training for undergraduate students at institutions, with the explicit goal of building research capacity while exposing students to the realities of scientific investigation. The WPI project is one of several new initiatives at the university funded through this program. For the students involved, the experience promises more than technical skill; it offers immersion in the full arc of a research problem, from reading the literature and formulating hypotheses to designing experiments, interpreting molecular data, and communicating findings. For the field, it represents an investment in the next generation of biomedical engineers at precisely the moment when questions about inflammation, coagulation, and vascular injury are becoming increasingly central to human health.
Mensah frames the dual purpose of the award in straightforward terms. The projects supported by the NIH, he notes, provide excellent training for students while also advancing fundamental understanding of human health. The work, he says, will establish an educational pipeline at WPI, enabling the university to train students in biology and prepare the next generation of biomedical engineers. If the laboratory succeeds on both fronts, the outcome will be twofold: a clearer molecular picture of how sepsis converts inflamed vessels into clot-forming surfaces, and a cohort of undergraduates who have already contributed to that discovery before beginning their professional careers. In a disease process as complex and deadly as sepsis-associated coagulation, progress on either front would be significant; progress on both, from a single laboratory, illustrates the model of research-integrated education that the grant is designed to support.
Subject of Research: NIH-funded undergraduate research into the molecular mechanisms linking sepsis-induced inflammation to blood clotting through glycocalyx degradation and von Willebrand factor release.
Article Title: Federal funding supports Worcester Polytechnic Institute student research into blood clots triggered by sepsis
Article References: Federal funding supports Worcester Polytechnic Institute student research into blood clots triggered by sepsis. (n.d.). Original publication
Image Credits: AI Generated
DOI: Not provided
Keywords: sepsis, blood clots, glycocalyx, von Willebrand factor, endothelial cells, Worcester Polytechnic Institute, NIH grant, undergraduate research, biomedical engineering, inflammation, stroke, Solomon Mensah
Cite Scienmag News
Drew Townsend. (September 22, 2026). NIH Grant Backs Undergraduate Research on Sepsis-Triggered Blood Clotting. Scienmag. https://scienmag.com/nih-grant-backs-undergraduate-research-on-sepsis-triggered-blood-clotting/
Drew Townsend. "NIH Grant Backs Undergraduate Research on Sepsis-Triggered Blood Clotting." Scienmag, 22 September 2026, https://scienmag.com/nih-grant-backs-undergraduate-research-on-sepsis-triggered-blood-clotting/. Accessed 22 September 2026.
Drew Townsend. "NIH Grant Backs Undergraduate Research on Sepsis-Triggered Blood Clotting." Scienmag. September 22, 2026. https://scienmag.com/nih-grant-backs-undergraduate-research-on-sepsis-triggered-blood-clotting/

