Penn Vet’s Andrew Vaughan works to uncover why some lungs rebound and others have lasting damage, and how to change that.
2 min. read
At the School of Veterinary Medicine, associate professor of biomedical sciences Andrew “Andy” Vaughan is a molecular and cellular biologist with a specific interest in lung regeneration. He seeks to understand why certain patients fully recover from severe respiratory infections, while others face debilitating damage.
Associate professor of biomedical sciences Andy Vaughan.
Vaughan and his team are looking at how injured lung cells miscommunicate during recovery, thereby driving inflammation and fibrosis. They are also determining mechanisms that can prevent or even reverse this damaging process. Vaughan continues to advance his vital work while navigating the shrinking federal support for research, an obstacle that underscores the urgent need to support biomedical breakthroughs that are making the world a more curative and healthier place.
Vaughan’s research is particularly focused on lung regeneration. “The lung sits in the middle ground of tissue repair: it’s much more regenerative than the brain or the heart, but much less regenerative than, say, the liver,” he says. “Some of these individuals who survive (COVID-19) recover to have completely normal lung function. Conversely, others deal with long-term, debilitating lung issues resulting from regenerative failures (e.g., scarring) in their lung tissue. We want to figure out how to prevent, or even reverse, these long-term consequences of severe lung injury.”
Vaughan highlights the research by a graduate student in his lab, Nick Holcomb. “Nick was curious to understand how injury to the epithelium lining of the lung, a common consequence of viral infection, impacts the behavior of lung fibroblasts, the cells that are responsible for the aforementioned scar tissue formation,” Vaughan says. “Nick showed that epithelial cells become ‘deranged’ by viral injury and secrete several factors that directly promote more pathologic changes in the nearby fibroblasts, causing them to recruit more immune cells, driving chronic and inappropriate inflammation that in turn leads to increased tissue fibrosis.”
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