Background: Aspirin exacerbated respiratory diseases (AERD) are characterized as an acute bronchospasm by ingestion of aspirin and heavy infiltration of eosinophils, which is contributed by altered synthesis of cycteinyl leukotrienes. Although the acquired Th2 response is apparently revealed in IgE - dependent asthma, but not obvious in AERD. Recently, IL-25, TSLP and IL-33 appears as key molecules of the innate Th2 response in allergic inflammation. Thus, we tried to reveal the relation of the innate Th2 molecules with development of AERD.
Methods and Materials: The level of IL-25, IL-33 and TSLP were measured in plasma before and after aspirin challenge to the subjects with AERD (n=18) and ATA (n=16) using an enzyme-linked immunosorbent assay (ELISA), and then normalized with plasma protein.
Results: The plasma level of IL-25, IL-33 and TSLP were comparable before aspirin challenge between AERD and ATA. After aspirin challenge, however, concentrations of IL-25 were robustly increased in AERD compared to those before aspirin challenge while did not change in ATA. The post challenge level of IL-25 was significantly higher in AERD more than that of ATA (0.34 pg/mg vs. 2.31 pg/mg; p=0.03), while those of IL-33 and TSLP were not changed. There was a significant correlation between concentrations of IL-25 and aspirin induced - fall rate of FEV1 in total subjects (r2=0.172, p=0.037).
Conclusions: Among the innate Th2 cytokines, IL-25, but not IL-33 and TSLP, is related with development of airway spasm after aspirin challenge, which suggest that IL-25 may be play roles in pathogenesis of AERD via modulation of Th2-type immune response.