title: Adipokine adipsin is associated with the degree of lung fibrosis in asbestos-exposed workers.
abstract: OBJECTIVE
  Asbestos-exposure causes an inflammatory response driven by alveolar macrophages that can lead to pulmonary fibrosis. In addition to classical inflammatory cytokines, macrophages produce adipokines which regulate the inflammatory response. We studied if adipokines are related to the degree of parenchymal fibrosis, impaired lung function and inflammation in asbestos-exposed subjects.
  
  
  METHODS
  Eighty-five males with moderate to heavy occupational exposure to asbestos and unexposed controls were studied. We measured plasma levels of adipokines adiponectin, adipsin, leptin and resistin, IL-6, IL-8, erythrocyte sedimentation rate (ERS), spirometry and D(L,CO). Degree of interstitial lung fibrosis (septal thickening, subpleural lines, parenchymal bands or honeycombing) was scored in classes 0-5 according to a validated scoring system. The subjects were divided into three groups: normal parenchymal finding (fibrosis class 0), borderline changes (classes 0.5-1.5) and fibrosis (i.e. asbestosis; classes 2-5).
  
  
  RESULTS
  Adipsin correlated positively with parenchymal fibrosis (rho=0.412, p<0.001) and there was a linear increasing trend of mean plasma adipsin levels among the three groups of asbestos-exposed subjects (from normal parenchymal finding to borderline changes and to fibrosis) (p<0.0001). Accordingly, plasma adipsin levels correlated positively with the extent of pleural plaques (r=0.245, p=0.043), and negatively with D(L,CO) (r=-0.246, p=0.023). Also, a positive correlation was found between adipsin and inflammatory markers ESR (r=0.315, p=0.008) and IL-6 (r=0.256, p=0.018).
  
  
  CONCLUSIONS
  Adipsin was associated with the degree of parenchymal fibrosis, impairment of pulmonary diffusing capacity and with inflammatory activity in asbestos-exposed subjects suggesting that adipsin may have a role in the pathogenesis or as a biomarker in asbestos-induced lung disease.
authors: Department of Respiratory Medicine, Tampere University Hospital, PL 2000, 33521 Tampere, Finland. sirpa.leivo-korpela@uta.fi
authors: Sirpa
authors: S
authors: Leivo-Korpela
authors: Lauri
authors: L
authors: Lehtimäki
authors: Riina
authors: R
authors: Nieminen
authors: Panu
authors: P
authors: Oksa
authors: Tuula
authors: T
authors: Vierikko
authors: Ritva
authors: R
authors: Järvenpää
authors: Jukka
authors: J
authors: Uitti
authors: Eeva
authors: E
authors: Moilanen
mesh_terms: D000704:Analysis of Variance; D001194:Asbestos / Q000633:toxicity*; D001195:Asbestosis / Q000175:diagnosis* / Q000209:etiology; D015415:Biomarkers / Q000378:metabolism; D001799:Blood Sedimentation; D011416:Complement Factor D / Q000378:metabolism*; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007378:Interleukins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects*; D011658:Pulmonary Fibrosis / Q000175:diagnosis* / Q000209:etiology; D014797:Vital Capacity / Q000502:physiology
chemical_list: D015415:Biomarkers; D007378:Interleukins; D001194:Asbestos; D011416:Complement Factor D