The prolonged retention of viscous airway secretions in the diseased lung (e.g., CF and COPD) can lead to recurring bacterial infections, resulting in a viscous, more purulent sputum . Increased mucus viscoelasticity may be attributed to extensive disulphide and lectin bonding, poor hydration, and/or excess concentrations of extracellular DNA or actin . In these situations, therapeutics have been used to reduce the viscosity of airway secretions to improve the rate of mucociliary clearance.
Mucolytic agents, such as N-acetylcysteine , guaifenesin , and diothiothreitol (DTT) , are used clinically and/or in vitro to reduce mucus viscosity. Lytic agents, such as recombinant human deoxynuclease I (rhDNase I, or Pulmozyme®) and Gelsolin® have also been effective in clearing viscous
airway secretions . Pulmozyme® enzymatically degrades extracellular DNA in human sputum . Gelsolin® severs noncovalent bonds between polymerized monomers of actin filaments. Gelsolin® may scavenge actin filaments released during the inflammation process, increasing the effectiveness of DNase I . Finally, the application of pulmonary surfactant to canine airways increased the mucus transport velocity nearly 400% in one study . The affect of using mucus-altering agents as adjuncts in gene delivery was investigated: the addition of mucus-altering agents produced similar transgene expression to mechanical mucus depletion .
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.