Sulfur dioxide-enhanced asthma susceptibility is involved with inhibition of bitter taste transduction in mouse lung.

Sulfur dioxide (SO) may induce asthma-like symptoms or worsen existing asthma, but the underlying mechanism is still unclear. In this study, the relationship between SO exposure, asthma development, and bitter taste transduction was analyzed using ovalbumin (OVA)-induced and SO-aggravated asthma models. The results showed that twenty-seven and twelve bitter taste receptors (Tas2rs) were detectable in mouse trachea and lung, respectively, and that all of them were nearly down-regulated in OVA-induced BALB/c and C57BL/6 asthmatic mice. SO exposure alone did not trigger a distinct asthma-like phenotype, but the combination of SO and OVA allergen caused more severe asthma symptoms in mice including enhanced inflammatory cells infiltration, thickened airway walls, increased mucus secretion, and elevated expression of proinflammatory and Th2 cytokines (TNF-α, IL-4, IL-5, IL-13). Furthermore, SO enhanced the transcriptional repression of Tas2rs in OVA-induced asthmatic mice. These results indicated that the occurrence of mice asthma was correlated with the inhibition of bitter taste transduction, and more severe airway inflammation and injury were accompanied with an enhanced inhibition of bitter taste transduction. Our findings suggest that SO inhalation may amplify Th2 inflammatory responses in the lung of asthmatic mice by inhibiting bitter taste transduction, and thereby exacerbate asthma symptoms.