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Mucus production in dust mite-related asthma explained

New research describes how signalling pathways in airway epithelial cells drive mucus production in asthma after stimuli from environmental triggers such as allergens (i.e. house dust mites), viruses or cigarette smoke. The same pathway was found to be responsible for activating excessive mucus in chronic obstructive pulmonary disease (COPD).
Increased mucus production is a common sign of inflammatory airway disease, such as asthma and COPD. In these conditions excess mucus production is likely to be responsible for acute flare-ups and a feature of chronic symptoms. In COPD the overpopulation of mucus cells in the small airways may be the cause of patient's distress, while reports of mucus plugging and thickening are typical in autopsies on asthma patients. The fact that both diseases can exist in one patient makes control of mucus production a major goal in therapeutic treatment. However, to date there is no specific and effective treatment for controlling airway mucus levels.

In addressing the cause of excessive mucus production there is clinical evidence that environmental stimuli from allergens (such as from house dust mites), viruses and cigarette smoke, can lead to immune cell production of IL 13. IL13 is a cytokine secreted by many cell types and known as the critical driver for mucus production. Recent research reports that excessive mucus is most probably due to increased biosynthesis and secretion of mucins, which are the major macromolecular constituents of airway mucus. Control of the increase of mucins is a target for research, however, the molecular signalling that begins the cascade of events towards excessive mucus production in the airways has previously been poorly defined.

Now in 2012, a breakthrough has been made. Experimental research describes evidence of an epithelial pathway {calcium-activated chloride channel (ClCA) genes} that, in the scientists' word, 'may fulfil a critical role for the development of mucous cell metaplasia'. In asthma, mucous cell metaplasia is responsible for the transformation of normal airway mucosa into a thickening mucosa with a high density of airway goblet cell population. Goblet cells hold mucus and are an essential part of airway cell population, but with an overabundance, or in the wrong place, goblet cells can cause excessive mucus.

The authors of this paper not only describe a new pathway by reporting; 'Here, we define a signalling pathway from chloride channel calcium-activated 1 (CICA1) to MAPK13 that is responsible for IL13 - driven mucus production in human epithelial cells', but they also give hope for a remedy to millions of patients who suffer from asthma, COPD, or other inflammatory airway diseases that result in excessive mucus production.


'IL-13 induced airway mucus production is attenuated by MAPK13 inhibition', 'J. Clin.Invest.' Yael G. Alevy et al, doi: 10. 1172/JC164896, November 2012

On line lecture in epithelial cell structure

'The Role of Atoh1 in Mucous Cell Metaplasia', Yoshihisa Nakamura et al, 'International Journal of Cell Otolaryngology', Vol. 2012 (2012) Article ID 438609, 5 pages doi:10.1155/2012/438609