DNA-modulating drug attenuates lung inflammation in mice


Patients with cystic fibrosis (CF) suffer from chronic respiratory infections, primarily caused by Pseudomonas aeruginosa, which lead to airway inflammation and damage. Several recent studies have suggested that a specific type of immune cell, known as Th17 cells, produce the factor IL-17 to drive the inflammatory response in the setting of CF lung infection. In this issue of JCI Insight, Jay Kolls and colleagues at the University of Pittsburgh demonstrate that bromodomain and extraterminal domain (BET) inhibitors, a class of drugs that alter DNA architecture and change gene expression, attenuate CF lung inflammation. Using immune cells isolated from CF patient lungs, Kolls and colleagues showed that BET inhibitors suppressed the response to Th17 cells as well as the release of inflammatory factors from Th17 cells. Moreover, in a mouse model of lung infection, BET inhibitor treatment decreased lung inflammation without promoting infection, indicating that BET inhibitors could potentially be used to treat CF patients.



Antiinflammatory effects of bromodomain and extraterminal domain inhibition in cystic fibrosis lung inflammation


Jay K. Kolls
Children's Hospital of Pittsburgh
Email: [email protected]

View this article at: http://insight.jci.org/articles/view/87168?key=28c129abe75d8548bd71

JCI Insight is the newest publication from the American Society of Clinical Investigation, a nonprofit honor organization of physician-scientists. JCI Insight is dedicated to publishing a range of translational biomedical research with an emphasis on rigorous experimental methods and data reporting. All articles published in JCI Insight are freely available at the time of publication. For more information about JCI Insight and all of the latest articles go to http://www.insight.jci.org.

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