PT - JOURNAL ARTICLE AU - Sharon Wong AU - Zaridatul Ibrahim AU - Peter Wark AU - Maria Sukkar TI - Potential role of SPARC, a downstream mediator of TGF-b in chronic airways disease AID - 10.1183/13993003.congress-2015.PA904 DP - 2015 Sep 01 TA - European Respiratory Journal PG - PA904 VI - 46 IP - suppl 59 4099 - http://erj.ersjournals.com/content/46/suppl_59/PA904.short 4100 - http://erj.ersjournals.com/content/46/suppl_59/PA904.full SO - Eur Respir J2015 Sep 01; 46 AB - Aim: Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein, known to play a key role in lung development and tissue remodeling. SPARC is also a downstream mediator of the pro-fibrotic and immunomodulatory cytokine TGF-b. Considering airway remodelling is a hallmark of both asthma and chronic obstructive pulmonary disease (COPD) and is driven by an aberrant inflammatory and fibrotic response, we seek to understand the role of SPARC in the pathogenesis of asthma and COPD. We determined whether airway epithelial cells express SPARC under baseline conditions and following stimulation with TGF-b; and whether rhSPARC modulates airway epithelial cell inflammatory and remodelling responses.Methods: SPARC protein was measured in BAL fluids obtained from healthy, asthmatic and COPD subjects by ELISA. Human primary airway epithelial cells (pAECs) or 16-HBE cells (monolayer) were stimulated with TGF-b1 (0.1-10ng/mL) or rhSPARC (0.1-10mg/mL). Cell-associated SPARC protein expression was determined by western blot while soluble SPARC in culture supernatants was determined by ELISA. Cytokine (IL6, IL1a and GM-CSF) and chemokine CCL20 production were measured by ELISA.Results: Preliminary data suggested that SPARC protein levels were elevated in the BAL fluid of COPD but not asthmatic subjects, compared to healthy control subjects. TGF-b1 upregulated SPARC expression in pAECs, although this was not observed in 16-HBE cells. Preliminary results also suggested that rhSPARC augment IL-6 production in pAECs, but further studies are required to confirm this.Conclusion: Our preliminary results suggest a possible role for SPARC in COPD pathogenesis, and this warrants further study.