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Lookup NU author(s): Dr James Garnett, Erin Baker
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For over 50 years, glucose has been recognised to cross the lung epithelial barrier and be transported by lung epithelial cells. However, until recently, research into these processes focused on their effects on lung liquid volume. Here, we consider a newly identified role for pulmonary glucose transport in maintaining low airway surface liquid (ASL) glucose concentrations and propose that this contributes to lung defence against infection. Glucose diffuses into ASL via paracellular pathways at a rate determined by paracellular permeability and the transepithelial glucose gradient. Glucose is removed from ASL in proximal airways via facilitative glucose transporters, down a concentration gradient generated by intracellular glucose metabolism. In the distal lung, glucose transport via sodium-coupled glucose transporters predominates. These processes vary between species but universally maintain ASL glucose at 3-20-fold lower concentrations than plasma. ASL glucose concentrations are increased in respiratory disease and by hyperglycaemia. Elevated ASL glucose in intensive care patients was associated with increased Staphylococcus aureus infection. Diabetic patients with and without chronic lung disease are at increased risk of respiratory infection. Understanding of mechanisms underlying lung glucose homeostasis could identify new therapeutic targets for control of ASL glucose and prevention and treatment of lung infection.
Author(s): Garnett JP, Baker EH, Baines DL
Publication type: Review
Publication status: Published
Journal: European Respiratory Journal
Year: 2012
Volume: 40
Issue: 5
Pages: 1269-1276
Print publication date: 01/11/2012
Online publication date: 09/08/2012
Acceptance date: 19/07/2012
ISSN (print): 0903-1936
ISSN (electronic): 1399-3003
URL: http://dx.doi.org/10.1183/09031936.00052612
DOI: 10.1183/09031936.00052612
PubMed id: 22878875
