Older adults are more likely to die from lung injury and acute respiratory distress syndrome than their younger counterparts, often due to inflammation and fluid accumulation (edema) that leads to reduced lung function and low blood oxygen levels. Alveolar epithelial type 2 (AE2) cells, found in the area of the lung where exchange of gases takes place, play a crucial role in normal lung function and recovery after injury. These cells produce and secrete a compound (surfactant) that prevents the balloon-like structure in the lungs (alveoli) from collapsing during breathing. Edema and inflammation can cause surfactant to inactivate, which may contribute to collapse of the alveoli. In addition, changes in surfactant protein expression can increase the severity of lung disease or injury.
Previous research suggests that the AE2 cells in aged mice show signs of senescence. Senescence is the process of deterioration, reduced function and a decrease in cell proliferation that occurs with aging. Cell proliferation is critical for regeneration and repair after an injury. However, “the consequences of AE2 cell senescence on the progression and regeneration of [acute lung injury] in elderly patients remains unknown,” authors of a new study wrote.
The researchers studied a mouse model of acute lung injury and recovery in young and old mice. The research team analyzed overall lung function, the number of AE2 cells in each lung, and surfactant function and properties. The lungs of the old mice showed signs of severe inflammation and edema compared to the young animals. While all of the young mice recovered from injury, 60% of the old animals did not recover. In addition, surfactant performance was impaired in sick and healthy old mice, suggesting that surfactant function declines with age even without the presence of disease. With acute lung injury, AE2 cell function was severely impaired in old compared with young mice and showed signs of senescence with limited proliferation and decline in surfactant protein expression and metabolisms.
Compared to young mice, the AE2 cells in the old mice “were less resistant to injury, leading to impaired surfactant metabolism, increased inflammation, cell senescence and decreased regeneration in [acute lung injury] of old mice—factors that all support a worse pathology and limited survival in [acute lung injury] with advancing age,” the researchers wrote. “We show that [acute lung injury] promotes cell senescence and limits regenerative capacity in AE2 in old mice.”
Read the full article, “Aging impairs alveolar epithelial type II cell function in acute lung injury,” published in the American Journal of Physiology-Lung Cellular and Molecular Physiology. It is highlighted as one of this month’s “best of the best” as part of the American Physiological Society’s APSselect program. Read all of this month’s selected research articles.
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