Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" Effect of neutrophil elastase and its inhibitor EPI-hNE4 on transepithelial sodium transport across normal and cystic fibrosis human nasal epithelial cells. | Prulière-Escabasse et al. Respiratory Research 2010 11 141 http content 11 1 141 RESPIRATORY RESEARCH RESEARCH Open Access Effect of neutrophil elastase and its inhibitor EPI-hNE4 on transepithelial sodium transport across normal and cystic fibrosis human nasal epithelial cells irnir io Dri iliora-Pcr-Ti cco1 2 3 hricf ino r lciri i4 5 6 íClrorirMra i iTỉrinÌTỉi IV7 Andre oefe1 2 3 Pcfdlo Pcr i iHior8 9 Viiginie riulièie Escabasse Ciiiistine Cleiici Giégoiie vuagniaux Andie Coste Estelle Escudiei Carole Planes10 11 Abstract Background Hyperactivity of the epithelial sodium Na channel ENaC and increased Na absoiption by aiiway epithelial cells leading to aiiway surface liquid dehydration and impaired mucociliaiy clearance are thought to play an important iole in the pathogenesis of cystic fibrosis CF pulmonaiy disease. In aiiway epithelial cells ENaC is constitutively activated by endogenous tiypsin-like seiine pioteases such as Channel-Activating Pioteases CAPs . It was iecently iepoited that ENaC activity could also be stimulated by apical tieatment with human neutiophil elastase hNE in a human aiiway epithelial cell line suggesting that hNE inhibition could represent a novel therapeutic approach foi CF lung disease. Howevei whethei hNE can also activate Na ieabsoiption in piimaiy human nasal epithelial cells HNEC fiom control oi CF patients is cuiiently unknown. Methods We evaluated by shoit-ciicuit cuiient sc measurements the effects of hNE and EPI-hNE4 a specific hNE inhibitoi on ENaC activity in piimaiy cultures of HNEC obtained fiom control 9 and CF 4 patients. Results Neithei hNE noi EPI-hNE4 treatments did modify sc in control and CF HNEC. Incubation with apiotinin a Kunitz-type seiine piotease inhibitoi that blocks the activity of endogenous CAPs decieased sc by and 54 in control and CF HNEC respectively. In control and CF HNEC pietieated with apiotinin hNE did significantly stimulate sc an effect which was blocked by .
