Targeting IκBNS in allergic asthma: Where it resides, matters

Abstract

The activity NF-κB, a pro-inflammatory transcription factor, and its complex modulation play a central role in in inflammatory airways disease such as allergic airway hyperresponsiveness. In a new study, Yokota and colleagues investigated IκBNS – an atypical inhibitor of NF-kB (IκB). Using elegant bone marrow chimera studies in mice, they found that IκBNS differentially modulated NF-κB activity in hematopoietic and non-hematopoietic cells. They also showed that by binding to the promoter region, this nuclear protein directly induced the MUC5AC gene in airway epithelial cells. This study enhances our understanding of how atypical IκB proteins work in regulating NF-κB activity and allergic airway conditions. It also emphasizes that targeting specific molecular pathways of airway inflammation may result in differential effects depending on the targeted tissue compartment. This is important in the search of novel asthma treatments and supports the fact that global anti-inflammatory approaches alone may not provide sufficient therapy.

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