title: Ceramide expression and cell homeostasis in chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Increased expression of ceramide has been detected in emphysema. Ceramide promotes autophagy and apoptosis, which concur with cellular homeostasis.
  
  
  OBJECTIVE
  To determine whether ceramide expression is associated with the development of chronic obstructive pulmonary disease (COPD) and with altered cellular homeostasis in lung parenchyma.
  
  
  METHODS
  We studied 10 subjects with severe COPD, 13 with mild/moderate COPD, 11 with idiopathic pulmonary fibrosis (IPF), 12 non-COPD smokers, and 11 nonsmoking controls. The immunoreactivity for ceramide along with markers of autophagy (LC3B), apoptosis (cleaved caspase-3), and cell proliferation (MIB1) was quantified in alveolar walls.
  
  
  RESULTS
  Ceramide expression was increased in COPD patients compared with control smokers and was related to the impairment of gas exchange but not to the degree of airflow limitation. In COPD, an important activation of apoptosis and autophagy pathways was observed, particularly in patients with severe disease, that was not counterbalanced by cell proliferation. Upregulation of ceramide was observed even in subjects with IPF in whom activation of apoptosis and autophagy was negligible and cell proliferation was instead the most prominent feature.
  
  
  CONCLUSIONS
  Ceramide expression, which is increased in COPD and even more so in IPF, appears to be neither specific nor related to COPD severity, probably representing a broader marker of lung damage. In contrast, apoptosis and autophagy are characteristics of the COPD pathology, particularly in its most severe stage.
authors.affiliation: Department of Environmental Medicine and Public Health, University of Padova, Via Giustiniani 2, Padua, Italy.
authors.forename: Maria C
authors.initials: MC
authors.lastname: Scarpa
authors.forename: Simonetta
authors.initials: S
authors.lastname: Baraldo
authors.forename: Emanuela
authors.initials: E
authors.lastname: Marian
authors.forename: Graziella
authors.initials: G
authors.lastname: Turato
authors.forename: Fiorella
authors.initials: F
authors.lastname: Calabrese
authors.forename: Marina
authors.initials: M
authors.lastname: Saetta
authors.forename: Piero
authors.initials: P
authors.lastname: Maestrelli
mesh_terms: D000368:Aged; D001343:Autophagy / Q000502:physiology; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation; D002518:Ceramides / Q000378:metabolism*; D005260:Female; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology*; D012907:Smoking; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism
chemical_list: D015415:Biomarkers; D002518:Ceramides; C502070:MAP1LC3B protein, human; D008869:Microtubule-Associated Proteins; C513496:MIB1 ligase, human; D044767:Ubiquitin-Protein Ligases; D053148:Caspase 3