OBJECTIVE/HYPOTHESIS: Through human leukocyte antigen-DR (HLA-DR) and intercellular adhesion molecule-1 (ICAM-1) expression, nasal epithelial cells could actively participate in the chronic inflammation and eosinophil infiltration observed in nasal polyps. The objective of the study was to evaluate HLA-DR and ICAM-1 expression in polyp epithelium and in a culture model of polyp epithelial cells allowing ciliated and secretory differentiation. STUDY DESIGN: Prospective non-randomized controlled in vitro study. METHODS: The in vitro HLA-DR and ICAM-1 expression was studied under basal conditions or after exposure to interferon-gamma, transforming growth factor-beta1, lipopolysaccharide, dexamethasone, or cetirizine. HLA-DR and ICAM-1 expression was investigated in situ by immunohistochemical staining of polyps and in vitro by immunofluorescent staining of cell cultures. HLA-DR and ICAM-1 were localized in cultured cells by confocal microscopy. Cultured cells expressing HLA-DR and ICAM-1 were quantified by flow cytometry. RESULTS: Both HLA-DR and ICAM-1 showed significant immunostaining of nasal polyp epithelium. In nasal polyp epithelial cell cultures, less than 5% of cells were positive for HLA-DR whereas 40% were positive for ICAM-1 at day 3. In vitro, HLA-DR was mainly located in the cytoplasm and ICAM-1 predominated on the apicolateral cytoplasmic membrane. Comparison of in situ and in vitro results showed that well-differentiated and poorly differentiated cells predominantly expressed HLA-DR and ICAM-1, respectively. Interferon-gamma significantly increased HLA-DR and ICAM-1 expression, whereas transforming growth factor-beta1 significantly decreased HLA-DR expression and lipopolysaccharide significantly increased ICAM-1 expression. CONCLUSION: HLA-DR and ICAM-1 epithelial expression in nasal polyps in situ and in vitro and their in vitro modulation reinforce the active role of epithelial cells in chronic inflammatory diseases of the upper airways.
OBJECTIVE/HYPOTHESIS: Through human leukocyte antigen-DR (HLA-DR) and intercellular adhesion molecule-1 (ICAM-1) expression, nasal epithelial cells could actively participate in the chronic inflammation and eosinophil infiltration observed in nasal polyps. The objective of the study was to evaluate HLA-DR and ICAM-1 expression in polyp epithelium and in a culture model of polyp epithelial cells allowing ciliated and secretory differentiation. STUDY DESIGN: Prospective non-randomized controlled in vitro study. METHODS: The in vitro HLA-DR and ICAM-1 expression was studied under basal conditions or after exposure to interferon-gamma, transforming growth factor-beta1, lipopolysaccharide, dexamethasone, or cetirizine. HLA-DR and ICAM-1 expression was investigated in situ by immunohistochemical staining of polyps and in vitro by immunofluorescent staining of cell cultures. HLA-DR and ICAM-1 were localized in cultured cells by confocal microscopy. Cultured cells expressing HLA-DR and ICAM-1 were quantified by flow cytometry. RESULTS: Both HLA-DR and ICAM-1 showed significant immunostaining of nasal polyp epithelium. In nasal polyp epithelial cell cultures, less than 5% of cells were positive for HLA-DR whereas 40% were positive for ICAM-1 at day 3. In vitro, HLA-DR was mainly located in the cytoplasm and ICAM-1 predominated on the apicolateral cytoplasmic membrane. Comparison of in situ and in vitro results showed that well-differentiated and poorly differentiated cells predominantly expressed HLA-DR and ICAM-1, respectively. Interferon-gamma significantly increased HLA-DR and ICAM-1 expression, whereas transforming growth factor-beta1 significantly decreased HLA-DR expression and lipopolysaccharide significantly increased ICAM-1 expression. CONCLUSION: HLA-DR and ICAM-1 epithelial expression in nasal polyps in situ and in vitro and their in vitro modulation reinforce the active role of epithelial cells in chronic inflammatory diseases of the upper airways.
Authors: D S Lazard; A Moore; V Hupertan; C Martin; V Escabasse; P Dreyfus; P-R Burgel; S Amselem; E Escudier; A Coste Journal: Allergy Date: 2009-02-24 Impact factor: 13.146
Authors: Jingwei Xin; Hui Sun; Hong Kong; Lin Li; Jun Zheng; Chunxia Yin; Yang Cao; Yunxiao Jia; Chaoxu Li Journal: Mol Med Rep Date: 2015-01-09 Impact factor: 2.952
Authors: Hahn Jin Jung; Yu Lian Zhang; Dong Kyu Kim; Chae Seo Rhee; Dong Young Kim Journal: Allergy Asthma Immunol Res Date: 2019-11 Impact factor: 5.764