Researchers have found that a protein called interleukin-15 plays a key role in lung damage caused by cigarette smoke and influenza virus infection.
Researchers have now analyzed the mechanisms that promote the decline in lung health with a special focus on the role of retinoic acid, a metabolite of vitamin A (retinol) that is known to have a key role in lung tissue development, maintenance and repair. The team also assessed the possible link between retinoic acid and IL-15.
Using mice models, researchers found that both long-term exposure to cigarette smoke and influenza virus infection decrease retinoic acid signaling by induction of IL-15, which in turn, significantly attenuates a retinoic acid receptor called retinoic acid receptor beta (RAR-beta). The team also reported that RAR-beta can be further attenuated by a combination of the two factors, viral infection and cigarette smoking exposure. In the absence of IL-15, RAR-beta expression is increased.
Researchers concluded that retinoic acid signaling is significantly decreased in mice lungs due to cigarette smoke exposure and influenza virus infection. IL-15 specifically decreases RAR-beta expression and restoration of the protective function of retinoic acid could represent a potential new therapeutic strategy to decrease lung injury in patients with emphysema and COPD.