Examining asthma with human lung-on-a-chip technology
Researchers at Penn Engineering developed an ‘asthma-on-a-chip’ system that mimics the mechanical stresses experienced by human airways during an asthma attack. The innovation enables scientists to probe how unhealthy lung tissue responds to compression in ways previously impossible to observe directly in patients.
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A bioengineered “asthma-on-a-chip” platform. (Image: Courtesy of Penn Engineering)
When an asthma attack strikes, the body turns against one of its most essential functions. Breathing becomes difficult, creating panic and increased inflammation. For millions of people living with asthma, the sensation can feel like trying to breathe through a straw.
According to Dan Huh, professor of bioengineering in the School of Engineering and Applied Science, much of what scientists still don’t understand about asthma may come down to something surprisingly physical.
“Asthma changes the lung, and not for the better,” Huh says. “It damages and reshapes airways over time. We tend to blame inflammation for it, but our work shows that the physical force of an airway squeezing shut may be just as important in understanding what drives those changes.”
In a new paper published in Nature Biomedical Engineering, Huh, together with lead author Jungwook Paek, a former postdoctoral researcher in Huh’s lab who is now an assistant professor of electrical and computer engineering at Binghamton University, and colleagues have developed a bioengineered “asthma-on-a-chip” system that recreates the mechanical stresses experienced by human airways during an asthma attack.
The platform allows scientists to observe how diseased lung tissue responds to physical compression in ways previously impossible to study directly in patients.
In healthy lungs, the airways widen and narrow freely with every breath. In asthmatic lungs, that flexibility is gradually lost. Beyond the familiar episodes of sudden narrowing, the airways themselves undergo lasting structural changes. Most notably, their walls thicken and stiffen as collagen builds up within them through a process known as airway remodeling. The resulting stiffer, narrowed airways are harder to keep open and respond poorly to standard medications, becoming a hallmark of the most severe and persistent forms of the disease. For decades, this remodeling was attributed almost entirely to chronic inflammation.
“Inflammation has long been seen as the main driver of asthma, and most therapies are built around the idea of controlling it,” says Huh. “The fact that asthma remains a major clinical challenge tells us we are missing part of the picture. One thing we know for certain is that the airways in asthmatic lungs constrict frequently. Yet we understand surprisingly little about how this defining mechanical feature affects the pathophysiology of the disease.”
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