11 Jun Alveolar telomeres may be secret to stopping emphysema before it begins
A recent scientific study carried out at the University of John’s Hopkins linked telomere dysfunction in alveolar cells to the appearance of idiopathic pulmonary fibrosis and emphysema.
The study tested the alveolar epithelial and stromal cells in the lungs of a group of mice with short telomeres. The researchers intentionally deleted telomere strands from the shelterin complex and observed as the mice’s bodies reacted. Quickly the type 2 alveolar epithelial cells (AEC2s), the stem-cell containing cells, became senescent. The mice’s immune systems responded to the dysfunction of the AEC2s cells by showing increased inflammation and vulnerability to idiopathic pulmonary fibrosis and emphysema, two diseases which would have normally been controlled by AEC2s with healthy telomeres.
The results show that alveolar stem cell failure leads to inflammation in the lungs and later idiopathic pulmonary fibrosis and emphysema in the lungs. The shortening of telomeres and later senescence of alveoli cells is the same biological dysfunction that smokers who develop emphysema experience.
The discovery of the role of telomeres in the onset of these fatal lung diseases is a good sign for the medical community. Now scientists can target efforts to lengthening alveoli stem cell telomeres in an effort to prevent emphysema and rather than trying to combat the disease once it has already set in.