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Inflammatory molecule involved in development of chronic obstructive pulmonary disease

() is characterized by poor airflow due to the breakdown of lung tissue, mucus accumulation and airway dysfunction. Development of is most commonly associated with smoking tobacco, however, it also occurs after acute respiratory infections such as influenza. It is unclear how prior leads to COPD.

In the current issue of the Journal of Clinical Investigation, Michael Holtzman and colleagues at the Washington University School of Medicine report that expression of an inflammatory molecule, interleukin-33 (IL-33), is increased in the airways of both a mouse model of viral-induced COPD and humans with COPD. Increased IL-33 was associated with an increase in mucus production, and expression of other COPD-implicated genes.

The authors found in their mouse model that expression of the gene encoding IL-33 was localized to a population of lungs cells that were induced in the airway after viral infection. These results lay the groundwork for potential therapeutic strategies aimed at preventing COPD after acute lung infection.

TITLE: Long-term IL-33-producing epithelial progenitor cells in chronic obstructive lung disease


J Clin Invest. doi:10.1172/JCI65570.

Journal of Clinical Investigation