Changes of T-helper type 1/2 cell balance by anticholinergic treatment in allergic mice

Background Anticholinergic drugs or vidian neurectomy can alleviate the symptoms of allergic rhinitis. Objective To show that inhibition of the cholinergic nerve influences the balance of T-helper type 1 and 2 cells in allergic rhinitis mice. Methods Twenty-four mice were randomly allocated to 1 of 4 groups: control, model, model with ipratropium bromide treatment, and model with 6-hydroxydopamine treatment. Allergic model-treated mice were sensitized with ovalbumin. Evaluation of allergic symptoms was recorded according to a symptom score. Ovalbumin serum IgE was measured by enzyme-linked immunosorbent assay. Expression of interleukin-4, interferon-γ, forkhead box P3, substance P, and vasoactive intestinal peptides was detected by immunohistochemistry and imaging analysis. Results Symptoms in allergic mice were significantly alleviated by ipratropium bromide. Ovalbumin serum IgE and eosinophils of nasal mucosa were significantly decreased. Interleukin-4 expression level was significantly higher in the allergic model group than in the control group and significantly decreased by ipratropium bromide (P < .05). In contrast, the expression of forkhead box P3 was lower in the allergic model group than in the control group and increased with treatment by ipratropium bromide (P < .05). Conversely, interferon-γ expression was not changed by anticholinergic treatment in the nasal mucosa of allergic mice. Expression of substance P and vasoactive intestinal peptide was significantly increased in allergic mice and decreased by ipratropium bromide. Sympathetic denervation did not change the expression of interleukin-4, interferon-γ, forkhead box P3, substance P, and vasoactive intestinal peptide. Conclusion inhibition of the cholinergic nerve not only alleviated symptoms of allergic rhinitis by inhibiting the impulse of the parasympathetic nerve but also modulated the T-helper type 2–predominant immune reaction, expression of neuropeptides, and related inflammation factors.