The role of pendrin in the airways: Links with asthma and copd

Abstract

Interleukin (IL)-4 and IL-13 are related cytokines correlated with type 2 immunity involved in the pathogenesis of bronchial asthma. Pendrin is induced by IL-4 or IL-13 in airway epithelial cells and is highly expressed in the lung tissues of asthma model mice or asthma patients. The signal transducer and activator of transcription (STAT) 6, the critical transcriptional factor for IL-4 or IL-13 signals, is required for IL-4- or IL-13-induced pendrin expression. Although the pathological roles of pendrin have been confirmed by the analyses of model mice, the underlying mechanisms are still unclear. Furthermore, pendrin has a potential to be correlated with other pulmonary diseases- chronic obstructive pulmonary disease, environmental chemical compound-exposed diseases or infectious diseases. In addition to these detrimental effects in pathological settings, the physiological role of pendrin in the lung, such as promoting antimicrobial activity, may be protective. Thus, whereas pendrin inhibition appears as a promising therapeutic strategy to treat asthma and other chronic respiratory diseases, it will be important to evaluate the effect of this inhibition in the lungs and other organs.