A new study in mice, by researchers at the University of Colorado Anschutz Medical Campus, reveals that intense light activates proteins shown to protect against lung damage. Their findings may pave the way for treating acute lung injury and lung diseases.

Their study is published in the American Journal of Physiology-Lung Cellular and Molecular Physiology, in a paper titled, “Intense light elicited alveolar type 2 specific circadian PER2 protects from bacterial lung injury via BPIFB1.”

“Acute lung injury has a mortality rate of 40%,” explained Tobias Eckle, MD, the study’s lead author and professor of anesthesiology at the University of Colorado School of Medicine. “No specific therapy exists, and novel treatment options are needed.”

“Circadian amplitude enhancement has the potential to be organ protective but has not been studied in acute lung injury (ALI),” the researchers wrote. “Consistent light and dark cycles are crucial for the amplitude regulation of the circadian rhythm protein Period 2 (PER2). Housing mice under intense instead of ambient light for one week (Light: Dark cycle:14h:10h), we demonstrated a robust increase of pulmonary PER2 trough and peak levels, which is consistent with circadian amplitude enhancement. A search for the affected lung cell type suggested alveolar type 2 (ATII) cells as strong candidates for light induction of PER2.”

If the protein was deleted in a specific lung cell known as the alveolar type 2 cell, acute lung injury was fatal. If the protein was not deleted, 85% of the mice survived.

The researchers also observed that intense light therapy reduced lung inflammation or improved the function of the alveolar barrier in lung infections.

At the same time, the researchers found that intense light stimulated production of the BPIFB1 protein, known to be anti-bacterial and secreted within the mucus membranes of the large airways. They believe this also likely plays a role in protecting the lungs.

Discovering that intense light can protect against lung damage, Eckle said, is important due to the lack of therapies currently available to treat the condition.

“If you develop lung injury there is essentially no good therapy left,” he said. “Our study has shown that intense light elicited lung-protective mechanisms could lead to new therapies even after the onset of acute lung injury in the future.”

“Together, our studies demonstrate that light elicited amplitude enhancement of ATII specific PER2 is a critical control point of inflammatory pathways during bacterial ALI,” concluded the researchers.