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Volume 42, Number 6, December 2009

Dioscorin protects tight junction protein expression in A549 human airway epithelium cells from dust mite damage

Ying-Hsien Ko, Kuo-Wei Lin, Jeng-Yuan Hsu, Lin-Shien Fu, Jao-Jia Chu, Chin-Shiang Chi

Received: June 20, 2006    Revised: January 21, 2007    Accepted: March 18, 2007   


Corresponding author:

Dr. Lin-Shien Fu, Department of Pediatrics, Taichung Veterans General Hospital, No. 160, Sec. 3, Chung Kong Rd., Taichung 407, Taiwan. E-mail:



Background and purpose: 

In addition to being an allergen, the trypsin activity of dust mite extract also destroys the tight junctions of bronchial epithelium. Such damage can lead to airway leakage, which increases airway exposure to allergens, irritants, and other pathogens. Dioscorin, the storage protein of yam, demonstrates anti-trypsin activity, as well as other potential anti-inflammatory effects. This study investigated the protective role of dioscorin for tight junctions.



The immunofluorescence stains of zonula occludens (ZO-1), E-cadherin (EC) and desmoplakin (DP) proteins were compared. A cultured A549 cell line was used as a control and A549 cells were incubated with mite extract 100 mg/mL for 16 h, with or without dioscorin 100 mg/mL pretreatment for 8 h and with dioscorin 100 mg/mL alone for 16 h. Western blot was performed to detect changes in ZO-1, EC, and DP in the treated A549 cell lines.



Loss of tight junction protein expression (ZO-1, EC, DP) was demonstrated after 16-h mite extract incubation. The defect could be restored if cells were pretreated with dioscorin for 8 h. In addition, dioscorin did not cause damage to the A549 cell lines in terms of cell survival or morphology. Western blot showed no change in the amount of tight junction protein under various conditions.


Dioscorin is a potential protector of airway damage caused by mite extract. 


Key words:

Cadherins; Desmoplakins; Dermatophagoides pteronyssinus; dioscorin protein, Dioscorea cayenensis; Tight junctions; zonula occludens-1 protein