BACKGROUND: Allergic rhinitis is a chronic nasal inflammatory disease mediated by an immunoglobulin E mediated process to environmental allergens. Although atopy is a potent predisposing risk factor for allergic rhinitis, local tissue susceptibilities are inevitable for disease expression. The nasal epithelium maintains tissue homeostasis by providing a physical barrier controlled by epithelial junctional proteins. However, the expression of epithelial junctional proteins has not been studied in patients with allergic rhinitis. We sought to elucidate the expression and the regulation of epithelial junctional proteins in the nasal epithelium of patients with allergic rhinitis. METHODS: The expression of E-cadherin and zonula occludens (ZO) 1 in epithelium of turbinate was measured by using real-time polymerase chain reaction, Western blot, and immunohistochemical assays, and was compared between control subjects and patients with allergic rhinitis. In addition, the expression levels of E-cadherin and ZO-1 were determined in cultured epithelial cell treated with interleukin (IL) 4, IL-5, tumor necrosis factor (TNF) alpha, and interferon gamma. RESULTS: The expression and the immunoreactivity of E-cadherin and ZO-1 were decreased in the nasal epithelium of patients with allergic rhinitis. Interestingly, the stimulation of cultured epithelial cells with IL-4, IL-5, and TNF-alpha resulted in downregulation of E-cadherin expression only in cultured epithelial cells of patients with allergic rhinitis, whereas E-cadherin expression in cultured epithelial cells of controls was not affected by stimulation with the same panel of cytokines. CONCLUSION: Decreased expression of epithelial junctional proteins was found in patients with allergic rhinitis. The disruption of epithelial integrity by IL-4, IL-5, and TNF-alpha in vitro indicated a possible role for these cytokines in the pathogenesis of patients with allergic rhinitis.
BACKGROUND:Allergic rhinitis is a chronic nasal inflammatory disease mediated by an immunoglobulin E mediated process to environmental allergens. Although atopy is a potent predisposing risk factor for allergic rhinitis, local tissue susceptibilities are inevitable for disease expression. The nasal epithelium maintains tissue homeostasis by providing a physical barrier controlled by epithelial junctional proteins. However, the expression of epithelial junctional proteins has not been studied in patients with allergic rhinitis. We sought to elucidate the expression and the regulation of epithelial junctional proteins in the nasal epithelium of patients with allergic rhinitis. METHODS: The expression of E-cadherin and zonula occludens (ZO) 1 in epithelium of turbinate was measured by using real-time polymerase chain reaction, Western blot, and immunohistochemical assays, and was compared between control subjects and patients with allergic rhinitis. In addition, the expression levels of E-cadherin and ZO-1 were determined in cultured epithelial cell treated with interleukin (IL) 4, IL-5, tumor necrosis factor (TNF) alpha, and interferon gamma. RESULTS: The expression and the immunoreactivity of E-cadherin and ZO-1 were decreased in the nasal epithelium of patients with allergic rhinitis. Interestingly, the stimulation of cultured epithelial cells with IL-4, IL-5, and TNF-alpha resulted in downregulation of E-cadherin expression only in cultured epithelial cells of patients with allergic rhinitis, whereas E-cadherin expression in cultured epithelial cells of controls was not affected by stimulation with the same panel of cytokines. CONCLUSION: Decreased expression of epithelial junctional proteins was found in patients with allergic rhinitis. The disruption of epithelial integrity by IL-4, IL-5, and TNF-alpha in vitro indicated a possible role for these cytokines in the pathogenesis of patients with allergic rhinitis.