TY - JOUR T1 - Comparative proteome analysis of lung tissue from patients with idiopathic pulmonary fibrosis (IPF) and non-specific interstitial pneumonia (NSIP) JF - European Respiratory Journal JO - Eur Respir J VL - 42 IS - Suppl 57 SP - P5122 AU - Martina Korfei AU - Ingrid Henneke AU - Philipp Markart AU - Daniel Von Der Beck AU - Clemens Ruppert AU - Poornima Mahavadi AU - Walter Klepetko AU - Ludger Fink AU - Silke Meiners AU - Oliver Krämer AU - Werner Seeger AU - Carlo Vancheri AU - Andreas Guenther Y1 - 2013/09/01 UR - http://erj.ersjournals.com/content/42/Suppl_57/P5122.abstract N2 - Among the idiopathic interstitial pneumonias (IIP), the two entities IPF and NSIP seem to be clinically related, but NSIP has a better outcome. The proteomic signatures which distinguish NSIP from IPF remain still elusive. We therefore performed comparative proteomic analysis of subpleural lung tissue from patients with sporadic IPF (n=14) and fibrotic NSIP (fNSIP, n=8) and organ donors (Controls, n=10), by using the innovative Difference in Gel Electrophoresis (DIGE) technique and MALDI-TOF-MS. The study revealed that the proteomic profiles of IPF and fNSIP were quite similar. Among the upregulated proteins in IPF and fNSIP were stress-induced genes involved in the ER stress-pathway, whereas downregulated proteins in IPF and fNSIP included antiapoptotic factors and antifibrotic molecules, such as serum amyloid P component, an inhibitor of fibrocyte differentiation. The direct comparison fNSIP versus IPF indicated upregulation of subunits of the proteasome activator complex (PSME1) and antioxidant enzymes of the peroxiredoxin family. In line with this, immunohistochemical analysis revealed induction and upregulation of peroxiredoxin1 and PSME1 in alveolar type-II cells in fNSIP-, but not in IPF lungs. We conclude, that only few protein expression changes exist between IPF and fNSIP, and that epithelial ER- and oxidative stress play a major role in the pathogenesis of both diseases. In contrast to IPF, intracellular clearance of reactive oxygen species and misfolded protein carbonyls seem to be enhanced in fNSIP due to enhanced expression of antioxidant acting proteins, and may explain the better outcome/survival in patients with fNSIP. ER -