TY - JOUR
T1 - Decreased expression of E-cadherin and ZO-1 in the nasal mucosa of patients with allergic rhinitis
T2 - Altered regulation of E-cadherin by IL-4, IL-5, and TNF-alpha
AU - Lee, Hyun Ji
AU - Kim, Byoungjae
AU - Im, Nu Ri
AU - Lee, Doh Young
AU - Kim, Ha Kyun
AU - Lee, Seung Hoon
AU - Lee, Heung Man
AU - Lee, Sang Hag
AU - Baek, Seung Kuk
AU - Kim, Tae Hoon
N1 - Funding Information:
Supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology and the Ministry of Science, Information and Communication Technology, and Future Planning (2010-0004094, 2011-0014068, 2014R1A1A1002131). This research was also supported by a Korea University grant, Korea and a Grant-in-Aid from the Department Foundation of Otorhinolaryngology-Head and Neck Surgery, Korea University College of Medicine
Publisher Copyright:
© 2016, OceanSide Publications, Inc., U.S.A.
PY - 2016/5/1
Y1 - 2016/5/1
N2 - 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. COPY
AB - 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. COPY
UR - http://www.scopus.com/inward/record.url?scp=84971596771&partnerID=8YFLogxK
U2 - 10.2500/ajra.2016.30.4295
DO - 10.2500/ajra.2016.30.4295
M3 - Article
C2 - 27216347
AN - SCOPUS:84971596771
SN - 1945-8924
VL - 30
SP - 173
EP - 178
JO - American Journal of Rhinology and Allergy
JF - American Journal of Rhinology and Allergy
IS - 3
ER -