tissue destruction 1 . Exacerbation is defined as an acute worsening of respiratory symptoms 1 that may be associated with the increase of airway inflammation mediated by neutrophils; lymphocytes; eosinophils; and the associated mediators, such as interleukin-8 (IL-8), regulated on activation, normal T cell expressed and secreted, and neutrophils elastase 2 . The causes of exacerbation are complex and mainly include respiratory, viral, or bacterial infections, and environmental pollution 3 , which lead to an increase in inflammatory burden and a decrease in protective defense by host immunity. In the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study 4 , which is a clinical observation on COPD patients over a period of 3 years, the exacerbation frequency appeared to be linked to prior history of exacerbation and severity of diseases. COPD patients with frequent exacerbations during the previous year tended to have higher susceptibility to exacerbations in the following years. What is the underlying mechanism to explain this frequent-exacerbation phenotype of COPD? What is breach of stability of airway inflammation and what triggers exacerbation? The co-existing eosinophilic inflammation and concomitant chronic diseases will be discussed (Figure
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Perng et al. (2017) studied this question.
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