Upregulation of nasal mucosal eotaxin in patients with allergic rhinitis during grass pollen season: effect of a local glucocorticoid.

BACKGROUND: Allergic rhinitis is a common disease characterized by infiltration of eosinophils into the nasal mucosa during the periods of symptoms. Among chemokines, which attract cells to the site of inflammation, eotaxin is relatively specific for eosinophils. OBJECTIVE: We examined the influence of grass pollen season on nasal eotaxin expression in patients with seasonal allergic rhinitis, as well as the effect of a nasal glucocorticoid on this eotaxin expression. METHODS: Nineteen patients with allergic rhinitis received treatment with either nasal beclomethasone (400 microgram/day) or placebo over a grass pollen season. In these patients, nasal biopsies were taken prior to and during the peak of the pollen season and stained immunohistochemically for eotaxin and EG2 + eosinophils. Five healthy subjects served as controls and gave nasal biopsies once prior to the pollen season. RESULTS: Prior to pollen season, there was no significant difference in nasal eotaxin expression between patients with allergic rhinitis and healthy subjects. Grass pollen season induced significant increase in eotaxin expression in placebo-treated (P = 0.04; n = 9) but not in beclomethasone-treated rhinitis patients (P = 0.8; n = 10). During peak grass pollen season, the eotaxin expression in placebo-treated patients was significantly higher compared with healthy subjects outside season (P = 0.03). There was no significant correlation between the expression of eotaxin and the number of EG2 + eosinophils in nasal mucosa. The serum levels of eotaxin in rhinitis patients remained stable over the pollen season. CONCLUSION: Expression of eotaxin in nasal mucosa of grass-pollen allergic rhinitis patients is upregulated during pollen season and treatment with a nasal glucocorticoid protects against this upregulation.

Randomized placebo-controlled study comparing a leukotriene receptor antagonist and a nasal glucocorticoid in seasonal allergic rhinitis.

Allergic rhinitis is an inflammatory disorder associated with local leukotriene release during periods of symptoms. Therefore, it has been suggested that antileukotrienes may be beneficial in the treatment of this disease. Leukotriene receptor antagonists have recently become available for asthma treatment, but little is known of their effects on allergic rhinitis. We have evaluated the effects of the leukotriene receptor antagonist zafirlukast versus placebo in patients with allergic rhinitis during the grass pollen season, using the nasal glucocorticoid beclomethasone dipropionate (BDP) as a positive treatment control. Thirty-three patients with seasonal allergic rhinitis were in a double-blind, double-dummy fashion randomized to treatments with oral zafirlukast (20 mg twice a day), intranasal beclomethasone dipropionate (200 microg twice a day), or placebo. The treatment was initiated 3 wk prior to the expected beginning of the grass pollen season. Patients completed a daily symptom-score list for sneezing, rhinorrhea, nasal itch, and nasal blockage during the 50-d treatment period. Nasal biopsies for quantification of local tissue eosinophilia (immunohistochemistry; EG2) were taken 1 mo before initiation of treatment and immediately after the peak of grass pollen season. Patients receiving treatment with zafirlukast had degrees of nasal symptoms similar to those in the placebo group, whereas the BDP group had significantly less symptoms compared with both treatments (p = 0.01 and p = 0.005, respectively). The numbers of activated eosinophils in the nasal tissue increased significantly during the pollen season in both the zafirlukast and the placebo groups, but not in the BDP group. These results obtained with a limited number of patients do not support any clinical efficacy of regular treatment with an oral antileukotriene in seasonal allergic rhinitis but rather favor the use of a nasal glucocorticoid.

An intranasal glucocorticoid inhibits the increase of specific IgE initiated during birch pollen season.

BACKGROUND: Recent in vitro findings show that glucocorticoids in combination with IL-4 can induce the synthesis of IgE, indicating that glucocorticoids may promote allergy. OBJECTIVE: A double-blind, placebo-controlled study was performed to evaluate the effect of an intranasal glucocorticoid on the levels of birch pollen-specific IgE antibodies in serum from patients with allergic rhinitis. METHODS: Eighteen patients with allergic rhinitis received treatment with an intranasal glucocorticoid (beclomethasone dipropionate, 400 microg/day) or placebo for 5 weeks, starting from the beginning of the birch pollen season. Blood samples for anti-birch IgE evaluation were taken before treatment was initiated and at 2 and 5 weeks after the beginning of the study. RESULTS: The beclomethasone group (n = 9) had significantly lower symptom scores when compared with the placebo group (n = 9) (0.86 +/- 0.26 vs 2.79 +/- 0.76, p value = 0.01). Both the treatment group and the placebo group showed a trend of an increase in anti-birch IgE levels 2 weeks after the beginning of the treatment (from 33.1 +/- 13.1 kU/L to 44.9 +/- 20.9 kU/L in the beclomethasone group and from 53.2 +/- 18.9 kU/L to 64.1 +/- 22.1 kU/L in the placebo group). Treatment with beclomethasone returned anti-birch IgE levels to baseline by the end of the study, whereas in the placebo group the anti-birch IgE levels continued to increase (final values, 33.1 +/- 11.9 kU/L vs 72.6 +/- 23.2 kU/L, respectively). The change in IgE antibody levels in the placebo group was significantly higher than that in the beclomethasone group. No statistically significant changes in total IgE or soluble CD23 levels were detected. CONCLUSION: We conclude that treatment with an intranasal glucocorticoid initiated at the beginning of the pollen season inhibits the induced increase in specific IgE.