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.
CAPE inhibited the production of eotaxin protein in stimulated human lung fibroblast cells in a dose-dependent manner. This activity is, at least, through STAT6 inhibition. We suggest that CAPE is a promising agent in controlling eotaxin secretion and subsequent eosinophils influx and may therefore have a potential role to play in treating allergic airway disease.
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