PT - JOURNAL ARTICLE AU - Sirpa Leivo-Korpela AU - Lauri Lehtimäki AU - Riina Nieminen AU - Panu Oksa AU - Tuula Vierikko AU - Ritva Järvenpää AU - Jukka Uitti AU - Eeva Moilanen TI - Adipokine adipsin is associated with the degree of parenchymal fibrosis in asbestos-exposed patients DP - 2011 Sep 01 TA - European Respiratory Journal PG - p3318 VI - 38 IP - Suppl 55 4099 - http://erj.ersjournals.com/content/38/Suppl_55/p3318.short 4100 - http://erj.ersjournals.com/content/38/Suppl_55/p3318.full SO - Eur Respir J2011 Sep 01; 38 AB - Asbestos causes an inflammatory response in the lungs, that can lead to pulmonary fibrosis called asbestosis. Most of the asbestos-exposed subjects show either normal or borderline parenchymal changes in high resolution computed tomography (HRCT). The significance of these borderline changes and their relation to pulmonary inflammation are not known. Adipokines regulate inflammatory responses and they are secreted by adipocytes and macrophages, while alveolar macrophages are known to be involved in asbestos-related lung inflammation. We assessed if adipokines are associated with the degree of pulmonary fibrosis in asbestos-exposed patients.We measured adipsin, adiponectin, leptin, resistin, IL-6 and IL-8 in blood, lung function, and thorax-HRCT in 85 men with a history of moderate or heavy occupational asbestos-exposure. The subjects were divided into three groups based on the HRCT-finding: normal, borderline or fibrosis.There was an increasing linear trend in the plasma levels of adipisin (p<0.0001) and adiponectin (p=0.0083) between the three groups, i.e. the more parenchymal changes on HRCT the higher the levels of adipsin and adiponectin. Adipsin levels correlated positively with the serum levels of IL-6 and the extent of pleural plaques on HRCT. Adipsin levels correlated negatively with TLCO, i.e. the higher the adipsin, the poorer the pulmonary transfer factor. Leptin or resistin were not associated with the degree of parenchymal fibrosis.In conclusion, adipokine adipsin was associated with the degree of parenchymal fibrosis and inflammatory activity in asbestos-exposed subjects, suggesting that adipsin may have a role in the pathogenesis of asbestos-induced lung injury.