The role of the NLRP3 inflammasome in the pathogenesis of airway disease

The incidences of respiratory diseases like asthma and Chronic Obstructive Pulmonary Disease (COPD) are increasing dramatically. Significantly, there are currently no treatments that can slow or prevent the relentless progression of COPD; and a sub-population of asthmatics are resistant to available therapies. What is more, currently prescribed medication has only minimal effect on the symptoms suffered in these patient groups. There is therefore an urgent need to develop effective drugs to treat these diseases. Whilst asthma and COPD are thought to be distinct diseases, it is currently believed that the pathogenesis of both is driven by the chronic inflammation present in the airways of these patients. It is thus hypothesised that if the inflammation could be attenuated, disease development would be slowed and symptoms reduced. It is therefore paramount to determine the pathways driving/propagating the inflammation. Recently there has been a growing body of evidence to suggest that the multimeric protein complex known as the Inflammasome may play key roles in the inflammation observed in respiratory diseases. The aim of this review is to discuss the role of the NLRP3 Inflammasome, and its associated inflammatory mediators (IL-1β and IL-18), in the pathogenesis of asthma and COPD.