Abstract
SummaryProlonged heat and sea salt aerosols pose a challenge for the mammalian airway, placing the protective airway surface liquid (ASL) at risk for desiccation. Thus, mammals inhabiting salt marshes might have acquired adaptations for ASL regulation. We studied the airways of the rice rat, a rodent that inhabits salt marshes. We discovered negligible Na+ transport through the epithelial sodium channel (ENaC). In contrast, carbachol induced a large Cl− secretory current that was blocked by the calcium-activated chloride channel (CaCC) inhibitor CaCCinhi-A01. Decreased mRNA expression of α, β, and γ ENaC, and increased mRNA expression of the CaCC transmembrane member 16A, distinguished the rice rat airway. Rice rat airway cultures also secreted fluid in response to carbachol and displayed an exaggerated expansion of the ASL volume when challenged with 3.5% NaCl. These data suggest that the rice rat airway might possess unique ion transport adaptations to facilitate survival in the salt marsh environment.
Highlights
The airway epithelium is a critical barrier to the external environment and is protected by a thin layer of fluid known as the airway surface liquid (ASL)
ASL volume and composition are regulated by active and passive epithelial cell ion transport that is in part dependent on the apical epithelial sodium channel (ENaC) (Chambers et al, 2007), the cystic fibrosis transmembrane conductance regulator (CFTR), and the calcium (Ca2+)-activated ClÀ channels (CaCC) (Frizzell and Hanrahan, 2012)
The loss of CFTR-mediated ClÀ and bicarbonate secretion in CF sets up an airway environment prone to infection, inflammation, mucous obstruction, ASL depletion, and impaired fluid secretion (Boucher, 2007; Pezzulo et al, 2012)
Summary
The airway epithelium is a critical barrier to the external environment and is protected by a thin layer of fluid known as the airway surface liquid (ASL). ASL volume and composition are regulated by active and passive epithelial cell ion transport that is in part dependent on the apical epithelial sodium channel (ENaC) (Chambers et al, 2007), the cystic fibrosis transmembrane conductance regulator (CFTR), and the calcium (Ca2+)-activated ClÀ channels (CaCC) (Frizzell and Hanrahan, 2012). The importance of these proteins in regulating ASL composition and volume has been repeatedly shown. CaCCmediated ClÀ transport regulates ASL volume acutely (Tarran et al, 2002), and in mice lacking the CaCC, TMEM16A, there is defective fluid secretion (Rock et al, 2009)
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