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The mucus bundles responsible for airway cleaning are retained in cystic fibrosis and by cholinergic stimulation

Artikel i vetenskaplig tidskrift
Författare Anna Ermund
Lauren N Meiss
Brendan Dolan
A. Bahr
N. Klymiuk
Gunnar C. Hansson
Publicerad i European Respiratory Journal
Volym 52
Nummer/häfte 2
ISSN 0903-1936
Publiceringsår 2018
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Språk en
Länkar dx.doi.org/10.1183/13993003.00457-2...
Ämnesord functional cftr channel, mucociliary transport, mucin, disease, trachea, model
Ämneskategorier Lungmedicin och allergi

Sammanfattning

The beneficial effect of anticholinergic therapy for chronic lung diseases such as chronic obstructive pulmonary disease (COPD) is well documented, although cholinergic stimulation paradoxically inhibits liquid absorption, increases ciliary beat frequency and increases airway surface liquid transport. Using pig tracheobronchial explants, we quantified basal mucus transport before as well as after incubation with the clinically used antimuscarinic compound ipratropium bromide (Atrovent) and stimulation with acetylcholine. As expected, surface liquid transport was increased by acetylcholine and carbachol. In contrast, the mucus bundles secreted from the submucosal glands normally transported on the cilia were stopped from moving by acetylcholine, an effect inhibited by ipratropium bromide. Interestingly, in pigs lacking a functional cystic fibrosis (CF) transmembrane conductance regulator (CFTR) channel, the mucus bundles were almost immobile. As in wild-type pigs, CF surface liquid transport increased after carbachol stimulation. The stagnant CF mucus bundles were trapped on the tracheal surface attached to the surface goblet cells. Pseudomonas aeruginosa bacteria were moved by the mucus bundles in wild-type but not CF pigs. Acetylcholine thus uncouples airway surface liquid transport from transport of the surface mucus bundles as the bundles are dynamically inhibited by acetylcholine and the CFTR channel, explaining initiation of CF and COPD, and opening novel therapeutic windows.

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