ENaC, iNOS, mucins, and wound healing in cystic fibrosis airway epithelial and submucosal cells

2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
Rashida Hussain ◽  
Hafiz Muhammad Umer ◽  
Maria Björkqvist ◽  
Godfried M. Roomans
Keyword(s):  
Cystic Fibrosis ◽  
Wound Healing ◽  
Airway Epithelial ◽  
Cystic Fibrosis Airway

scholarly journals Physiological Impact of Abnormal Lipoxin A4Production on Cystic Fibrosis Airway Epithelium and Therapeutic Potential

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Gerard Higgins ◽  
Fiona Ringholz ◽  
Paul Buchanan ◽  
Paul McNally ◽  
Valérie Urbach
Keyword(s):  
Cystic Fibrosis ◽  
Therapeutic Potential ◽  
Chloride Transport ◽  
Early Death ◽  
Airway Epithelial ◽  
Resolution Of Inflammation ◽  
Cystic Fibrosis Airway ◽  
Infection And Inflammation ◽  
Subsequent Activation ◽  
Physiological Impact

Lipoxin A4has been described as a major signal for the resolution of inflammation and is abnormally produced in the lungs of patients with cystic fibrosis (CF). In CF, the loss of chloride transport caused by the mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) Cl−channel gene results in dehydration, mucus plugging, and reduction of the airway surface liquid layer (ASL) height which favour chronic lung infection and neutrophil based inflammation leading to progressive lung destruction and early death of people with CF. This review highlights the unique ability of LXA4to restore airway surface hydration, to stimulate airway epithelial repair, and to antagonise the proinflammatory program of the CF airway, circumventing some of the most difficult aspects of CF pathophysiology. The report points out novel aspects of the cellular mechanism involved in the physiological response to LXA4, including release of ATP from airway epithelial cell via pannexin channel and subsequent activation of and P2Y11 purinoreceptor. Therefore, inadequate endogenous LXA4biosynthesis reported in CF exacerbates the ion transport abnormality and defective mucociliary clearance, in addition to impairing the resolution of inflammation, thus amplifying the vicious circle of airway dehydration, chronic infection, and inflammation.

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