Sulfur dioxide is a typical
air pollutant.
Sulfite, which is formed at the bronchial mucosa from inhaled
sulfur dioxide, might play a role in the exacerbation of
asthma. In this study, we investigated the effects of
sodium sulfite and its interaction with a house dust mite (Dermatophagoides pteronyssinus, Der p) on allergic sensitization and airway
inflammation. BALB/c mice were divided into four groups: control (n = 10), mite intranasal (mIN, n = 12),
sodium sulfite intranasal (sIN, n = 12) and mIN + sIN (n = 12). In non-control groups, the mice were sensitized on day 8 and day 15 with mite
allergen subcutaneously. Mite
allergen was then administrated intranasally from day 15 to day 22 in mIN and mIN+sIN groups.
Sodium sulfite was administrated in sIN and mIN + sIN groups intranasally from day 1 to day 22. Plasma Der p-specific
IgE,
IgG2a, lung histopathology and
cytokine levels (IL-5 and IFN-γ) were analyzed. In comparison between mIN (or sIN) and mIN + sIN group, Der p-specific
IgE levels were significantly higher in mIN + sIN group (p < 0.01). Besides, Der p-specific
IgG2a level was significantly lower in mIN + sIN group than mIN (or sIN) group (p < 0.01). The peribronchiolar, alveolar and total inflammatory scores were increased in the mIN + sIN group comparing with the control group (p < 0.05, p < 0.01, p < 0.01, respectively). Lung supernatant in mIN + sIN group has higher IL-5/IFN-γ ratio than control, mIN or sIN group (all p < 0.05). Our study concluded
sodium sulfite may enhance allergic sensitization as well as airway
inflammation in mite
allergen sensitized BALB/c mice.