Glucocorticoids and β2-agonists regulate the pathologic metabolism of hyaluronic acid in COPD.

摘要: Abstract Background and objective We have previously shown that airway smooth muscle cells (ASMC) from COPD patients exhibit an abnormal metabolism of hyaluronic acid (HA) exacerbations are associated with pro-inflammatory degradation HA. In the present study, we investigated effect glucocorticoids long-acting β 2 -agonists (LABA) on pathologic HA in COPD. Methods Primary cultures ASMC, established endo-bronchial biopsies patients, were treated LABA. Secretion was measured by ELISA synthase-1 (HAS-1) hyaluronidase-1 (HYAL-1) assessed RT-PCR western blotting. Furthermore, a cohort 97 underwent diagnostic bronchoscopy, identified 11 treatment-naive 13 inhaled corticosteroids (ICS) LABA prior to bronchoscopy. HA, HAS-1 HYAL-1 bronchoalveolar lavage (BAL) these hyaluronidase activity reverse zymography. Results The combination stimulated secretion high molecular mass ASMC patients. This increased expression reduced HYAL-1. drugs mediated via their specific receptors since it inhibited receptor antagonists. Patients ICS presented levels decreased BAL. Conclusions counteracts COPD, suggesting additional beneficial when used for treatment