Objective: To observe the effect of sulphur dioxide (SO2) inhalation on the pathogenesis of allergic rhinitis (AR) in mice, and investigate the toxic effect of SO2 on respiratory tract mucosa.
Methods: Fifty male Kunming strain mice were randomly allocated to five groups, i. e., control group, AR group and AR plus different concentrations of SO2 group (three sub-groups). Nasal cavity irrigating solution was gathered from nasal cavity, and blood from the orbital venous sinus after anesthesia The concentrations of IL-5 and IL-13 in the peripheral serum and nasal cavity irrigating solution were measured by ELISA. The number of eosinophils (EOS) per square millimeter in sinus mucosa was calculated by hematoxylin-eosin. The expression of SP-D in nasal mucosa was analyzed by immunohistochemistry technique.
Results: With increasing concentrations of SO2, the levels of IL-5 and IL-13 in the peripheral serum, and the density of Eos in sinus mucosa increased simultaneously. A positive correlation existed between the concentration of inhaled SO2 and the elevation of both IL-5, IL-13 and Eos infiltration in nasal mucosa. The coefficient correlation relatively were 0.894, 0.874, 0.894, 0.891 and 0.870 (P <0.01). The expression of SP-D in 56 mg/m3 and 112 mg/m3 SO2 groups was higher, while it was lower in 168 mg/m3 SO2 group (P < 0. 001).
Conclusions: The study showed that sulphur dioxide inhalation facilitates the onset of allergic rhinitis in mice. SO2-related Th2-derived cytokines as well as the infiltration of EOS in nasal mucosa help to aggravate the development of allergic rhinitis.
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