Type II Alveolar Epithelial Cells in Remodeled Areas of Idiopathic Pulmonary Fibrosis or Usual Interstitial Pneumonia - Abstract
In our previous study we showed that in normal areas of usual interstitial pneumonia (UIP), type II alveolar epithelial cells telomerase positive (AEC2T+) expression was
significantly inferior when compared to normal lung tissue (NLT). Nevertheless, the density of AEC2 was the same in both UIP and NLT. An inversely significant correlation
was observed between AEC2 density and AEC2 apoptosis in this area. These results led us to suggest that the pathogenesis of UIP after numerous mitoses is that AEC2 T-exhausts its telomeres and enters into apoptosis, in patients with small subpopulation of AEC2 T+. If this is correct, AEC2 T+ prevails in the remodeled areas of UIP. Thus, we
hypothesized that in remodeled areas, AEC2T+ is predominant.
Material and Methods: We studied 24 open lung biopsies (12 male and 12 female) from our previous study with IPF/UIP disease [4]. Immunohistochemistry (IHC) analysis was performed to identify AEC2 by surfactant A protein and anti-telomerase antibodies. AEC2 density and telomerase expression in the remodeled areas of UIP were assessed at different time points in ten fields using the point-count technique. Forced vital capacity (FVC) was measured by Collins’s computer spirometer in 15 patients
Results: The mean of AEC2 and with Telomerase did not present significant difference. There was a significant positive correlation between AEC2T+ density and FVC- %.
Conclusion: Our interpretation on the pathogenesis of IPF/UIP was confirmed by the predominance of AEC2T+. A positive correlation was found between AEC2T+ and FCV%