Aaron Morris Receives NIH MIRA Award to Advance Immune-engineering Approaches for Chronic Wounds

University of Michigan Biomedical Engineering Assistant Professor Aaron Morris has received a National Institutes of Health (NIH) Maximizing Investigators’ Research Award (MIRA) from the National Institute of General Medical Sciences (NIGMS). The award will support Dr. Morris’s research program aimed at understanding, and ultimately improving, why certain wounds fail to heal.

Two models, one challenge: wounds that don’t resolve

Chronic wounds affect millions of patients and can lead to serious complications, including infection and amputation risk in diabetes. Dr. Morris’s MIRA-supported work will focus on two types of chronic, non-resolving tissue damage:

• Diabetic skin wounds (modeled in animals with type 2 diabetes) to capture features relevant to hard-to-heal ulcers.
• The foreign body response to medical implants, a persistent inflammatory reaction to biomaterial implants that can lead to device failure.

“We’re going to study two different kinds of chronic wounds,” Dr. Morris said. “One is dermal wound healing in type 2 diabetic models—skin wounds that can simulate problems such as diabetic foot ulcers. The other is the foreign body response to implants.”

Dr. Morris emphasized that the foreign body response is widespread across implanted technologies, although its impact varies by device type, material, and where it is located in the body. “If an implant doesn’t quickly degrade, you can have a foreign body response,” he said. “It’s a chronic, non-healing wound that can’t fully resolve because there’s something in the way.”

In some applications, the consequences are particularly limiting. “Implantable sensors can become useless after a couple weeks, partially because of this response,” Dr. Morris noted. The reaction can also contribute to device failure over time, adding clinical risk, cost, and the burden of revision procedures.

Centering immune dysfunction—especially T cells

A major theme of the work is immune dysregulation: how immune cells behave differently in wounds that stall rather than repair. In diabetic wounds, this dysfunction is well recognized, but the precise mechanisms and timing remain incomplete.

Dr. Morris’s lab is particularly interested in T cells, including the balance between conventional T cells, which drive inflammation and pathogen defense, and regulatory T cells, which restrain harmful inflammation and can support repair. “Regulatory T cells are important for healing,” Dr. Morris said. “But exactly what they’re doing, and what the right balance is between regulatory and conventional T cells, is not well understood.”

To interrogate that balance, the team plans to use engineered biomaterials and delivery strategies to intentionally shift immune dynamics and measure what changes. “Our approach is to perturb the system and see what happens,” Dr. Morris said. “We’re going to deliver drug-loaded materials that reprogram conventional T cells into regulatory T cells, pushing that balance and seeing how it affects healing—whether it improves it, makes it worse, and how timing matters.”

The immediate goal is mechanistic insight, not a near-term clinical product. “If we learn how the immune balance controls healing, then we can think about translation later,” Dr. Morris said. “But the goal of this project is to perturb things and understand what’s happening.”

A second arm: “alarms” that may stay switched on

The MIRA’s flexible structure will also support a complementary line of investigation focused on innate immunity—the body’s early inflammatory response—and a class of molecules known as alarmins, also called damage-associated molecular patterns (DAMPs).

“Alarmins are really important early in wound healing,” Dr. Morris said. “They call the immune system and say, ‘We need inflammation,’ which is important. But if they’re chronically elevated, they may keep the alarm bells ringing too long, and that could be part of the problem.”

To understand how these signals evolve over time in chronic wounds, Dr. Morris’s lab plans to apply synthetic biology tools to create cell-based sensors that can report on the presence and level of these molecules inside wound environments. “We want to engineer cells with synthetic receptors for some of these alarmins,” Dr. Morris said. “We can put them into wounds as sensors to report on what’s happening over time.”

Building knowledge that enables new therapies

By pairing two wound contexts with immune-focused “perturb-and-measure” strategies, the team aims to uncover shared principles of chronic inflammation and stalled repair. Over time, those insights could inform new approaches—from smarter wound dressings to improved implant integration. “This project is less translationally oriented,” Dr. Morris noted. “It’s about trying to understand chronic wounds—what’s going wrong, and how immune dysfunction drives that outcome.”

What the NIH MIRA supports

The NIH Maximizing Investigators’ Research Award (MIRA R35) provides funding over five years to biomedical engineers for flexible, long-term research, with the goal of enabling more breakthroughs than would be possible through a series of discrete, project-by-project awards. The target audience includes Promising Early Stage Investigators (ESIs), as well as established investigators whose work aligns with the NIGMS mission.

MIRA’s scope broadly spans bioengineering, chemical engineering, drug development, and therapeutic advancement. Recent MIRA-supported grants have funded studies in tissue modeling, computational drug design, imaging technologies, and cellular behavior—all aimed at advancing human health.

The MIRA mechanism is designed to support a coherent research direction rather than a single tightly defined project. “A MIRA is program-based and is for the support for the overall space we’re working in and the contribution we can make,” Dr. Morris said.