Abstract
Introduction: Autophagy, derived from the Greek and meaning “self eating,” is a homeostatic mechanism which contributes to cellular homeostasis. The modulation of autophagy in alveolar macrophages (AM) has been explored in chronic obstructive pulmonary disease and evidence of impaired autophagy was found. Although autophagy may protect against the development of fibrosis, its role is still unknown in AM.
Aim : With this background, we evaluated the autophagic activity in AM obtained form the bronchoalveolar lavage fluid (BALF) of patients with Idiopathic Pulmonary Fibrosis (IPF). Beclin-1 and p62, markers autophagic activity, have been evaluated and correlated with markers of disease severity (forced vital capacity: FVC, and diffusion capacity: DLco).
Patients and methods: We have prospectively studied 48 IPF patients and 16 controls. The expression of beclin-1 and p62 in AM has been evaluated with real-time PCR.
Results: We found no differences in the m-RNA expression of the the two genes between the study groups. Although cigarette smoking influences autophagy in AM no differences were obseved in the levels of Beclin-1 and p62 in smokers compared to non-smokers. In addition, no correlation was observed with markers of disease severity.
Conclusion: We have studied, for the first time, AM isolated from BALF of IPF patients. Our preliminary results show that autophagy does not appear impaired, at the level of mRNA expression regarding beclin-1 and p62. Further study of autophagy gene expression is needed.
- © 2014 ERS