OBJECTIVES: To determine whether the chloride channel protein CLC-3 is upregulated in patients with allergic rhinitis (AR) and whether topical corticosteroid treatment decreases the expression of CLC-3. DESIGN: Histologic study. SETTING: Academic research. PATIENTS: Eighteen patients with AR were included in the study. MAIN OUTCOME MEASURES: Expression of CLC-3 was detected by immunohistochemistry and by reverse transcription-polymerase chain reaction before and at 4 weeks after treatment with the topical corticosteroid mometasone furoate. RESULTS: Strong CLC-3 expression was detected in epithelium and in submucosal glands. An increased presence of CLC-3 was demonstrated in nasal mucosa compared with that in normal nasal tissue. A statistically significant difference in CLC-3 gene expression level was found in nasal tissues before vs at 4 weeks after treatment with mometasone. CONCLUSIONS: CLC-3 may have a role in modulating the pathogenesis of AR. Decreased expression of CLC-3 may be the mechanism of action of corticosteroid treatment in controlling AR.
OBJECTIVES: To determine whether the chloride channel protein CLC-3 is upregulated in patients with allergic rhinitis (AR) and whether topical corticosteroid treatment decreases the expression of CLC-3. DESIGN: Histologic study. SETTING: Academic research. PATIENTS: Eighteen patients with AR were included in the study. MAIN OUTCOME MEASURES: Expression of CLC-3 was detected by immunohistochemistry and by reverse transcription-polymerase chain reaction before and at 4 weeks after treatment with the topical corticosteroid mometasone furoate. RESULTS: Strong CLC-3 expression was detected in epithelium and in submucosal glands. An increased presence of CLC-3 was demonstrated in nasal mucosa compared with that in normal nasal tissue. A statistically significant difference in CLC-3 gene expression level was found in nasal tissues before vs at 4 weeks after treatment with mometasone. CONCLUSIONS:CLC-3 may have a role in modulating the pathogenesis of AR. Decreased expression of CLC-3 may be the mechanism of action of corticosteroid treatment in controlling AR.