Protective Effects of Exogenous Surfactant Protein A in Allergic Rhinitis: A Mouse Model

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A mouse model of allergic rhinitis (AR) was prepared, and exogenous surfactant protein A (SP-A) was given by an intranasal route to study its mechanism and effects in the mice.


Sixty male BALB/c mice were randomly divided into a normal control group, a group with AR (AR group), and a group with AR that was given SP-A (treatment group).


A mouse model of AR was successfully established. Enzyme-linked immunoassay showed that the level of ovalbumin-specific immunoglobulin E in the AR group was significantly higher than those in the treatment and control groups (p < 0.05), whereas the levels were not significantly different (p > 0.05) between the treatment and control groups. Hematoxylin-eosin staining showed typical allergic injury of the nasal epithelium in the AR group, and the number of eosinophils that migrated into the nasal tissue in the AR group was significantly greater than those measured in the treatment and control groups (p < 0.05). Western blotting and real-time quantitative polymerase chain reaction testing revealed that the type 2 helper (Th2) cytokine (interleukin 4 and interleukin 5) levels were highest in the AR group, followed by the treatment and control groups, with significant differences between each of the groups (p < 0.05). Significant differences were found in the levels of nasal mucosa type 1 helper (Th1) cytokines (interferon γ, interleukin 12) among the AR, treatment, and control groups; the highest levels were found in the control group, and the lowest levels were detected in the AR group (p < 0.05).


Exogenous SP-A had a significant therapeutic effect in mice with AR, and its mechanisms of action included inhibition of the differentiation of Th2 cells in the nasal mucosa, reduced levels of Th2 cytokines, and increased levels of Th1 cytokines. Together, these effects corrected the Th1/Th2 imbalance, inhibited the increase of specific immunoglobulin E production, effectively reduced the symptoms of AR, and inhibited the development of AR.

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