A $3.3 million National Institutes of Health grant will allow University of Arizona Health Sciences researchers to characterize the unique immune response associated with emphysema, ultimately informing earlier and more personalized treatment approaches for COPD. 

Emphysema and chronic bronchitis are the two most common conditions that contribute to COPD, but the two diseases require distinctive approaches, according to Francesca Polverino, PhD, a BIO5 Institute member and associate professor in the UArizona College of Medicine – Tucson.

“People with emphysema cannot be encompassed under the same umbrella as other COPD patients because they present a completely different disease,” said Polverino. 

Unlike those with chronic bronchitis, emphysema patients exhibit autoimmune responses leading not only to loss of lung tissue, but also to loss of bone and muscle throughout their bodies. These patients are “falling apart systemically,” Polverino says, likely because of improper B cell responses.

B lymphocytes, a key part of the adaptive immune system, are white blood cells responsible for producing antibodies in response to foreign materials and harmful microbes. While the actions of B cells are essential to our protection against a variety of diseases, they sometimes incorrectly target our own tissues, leading to an autoimmune response.

Prior research by Polverino and others has shown that not all COPD patients – only those with emphysema – have prominent lung B cell responses, regardless of the degree of airflow limitation they experience. 

With this five-year grant from the NIH’s National Heart, Lung and Blood Institute, Polverino and her team will further explore the B cell immune responses in COPD patients, especially those with emphysema and heightened autoimmunity. They aim to identify biomarkers of emphysema B cell responses that are distinct from other types of COPD, allowing scientists and physicians to take a precision medicine approach to treating this chronic disease. 

“This research is the first brick of a wall because we really don’t know anything about the B cell response in these people,” Polverino said. “This work is very overdue.”

Once she correlates the extent of B cell activity with emphysema severity, Polverino plans to assess antibody production throughout the body, as emphysema can cause systemic (whole-body) problems. If her hypothesis is correct, Polverino expects that circulating off-targeted B cells, similar to that in the lung, will also correlate with emphysema severity.