Background: Nasal polyps in the nasal cavity and mucous discharge inside the maxillary sinus exhibit compressive stress on the nasal mucosal epithelium. However, there have been only a few studies on how compressive stress impacts the human nasal mucosal epithelium. Methodology: We investigated the effect of compressive stress on collective migration, junctional proteins, transepithelial electrical resistance, epithelial permeability, and gene expression in well-differentiated normal human nasal epithelial (NHNE) cells and human nasal polyp epithelial (HNPE) cells. Results: NHNE cells barely showed collective migration at compressive stress up to 150 mmH2 0. However, HNPE cells showed much greater degree of collective migration at a lower compressive stress of 100 mmH2 0. The cell migration of HNPE cells sub-jected to 100 mmH2 O compression was significantly decreased at day 3 and was recovered to the status prior to the compressive stress by day 7, indicating that HNPE cells are relatively more sensitive to mechanical pressure than NHNE cells. Compressive stress also increased transepithelial electrical resistance and decreased epithelial permeability, indicating that the compressive stress disturbed the structural organization rather than physical interactions between cells. In addition, we found that compressive stress induced gene expressions relevant to airway inflammation and tissue remodelling in HNPE cells. Conclusion: Taken together, these findings demonstrate that compressive stress on nasal polyp epithelium is capable of inducing collective migration and induce increased expression of genes related to airway inflammation, innate immunity, and polyp remo-delling, even in the absence of inflammatory mediators.
|Number of pages||10|
|Publication status||Published - 2021|
Bibliographical noteFunding Information:
This research was supported by the National Research Foundation of Korea (NRF) grants funded by the Ministry of Science, ICT (Information and Communication Technologies), and Future Planning (2016K1A1A2910779, 2018R1A2A3075287).
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