Background: Exposure to atmospheric pollutants is closely associated with the occurrence of allergic rhinitis (AR). However, the role of sulfur dioxide (SO₂) in promoting allergic inflammation in AR is poorly understood. Our study aims to investigate the effect of SO₂ on allergic inflammation in house dust mite (HDM)-sensitized mice.
Methods: Thirty mice were randomly divided into five groups: the control, AR model, AR model exposed to SO₂, AR model with long-term SO₂ exposure, and SO₂-treated control groups. Nasal symptom score was recorded. The serum HDM specific IgE (sIgE) was measured by enzyme-linked immunosorbent assay. Expression of Th1/Th2/Th17 cytokines in nasal mucosa was detected by immunohistochemistry and quantitative PCR. Expression of a low-affinity sIgE receptor (CD23) on B lymphocytes in nasal mucosa was assessed by immunofluorescence.
Results: SO₂ increased not only nasal symptom score but also the number of infiltrating eosinophils and expression of Th1/Th2/Th17 cytokines in nasal mucosa of HDM-sensitized AR mice. Furthermore, SO₂ increased the serum sIgE level in AR mice. However, long-term SO₂ exposure decreased the serum sIgE level in AR mice. Moreover, long-term SO₂ exposure decreased CD23⁺ B lymphocytes in the nasal mucosa.
Conclusion: SO₂ exposure aggravated nasal symptom, serum sIgE level, eosinophil infiltration, and Th1/Th2/Th17 inflammation in AR mice. However, the serum sIgE level could be lowered by long-term SO₂ exposure. This inhibitory effect of SO₂ on IgE production may be suppressed by CD23⁺ B lymphocytes.
Keywords: allergic rhinitis, air pollution, sulfur dioxide, inflammation