Intermittent hypoxia induces turbinate mucosal hypertrophy via upregulating the gene expression related to inflammation and EMT in rats

Purpose Chronic intermittent hypoxia (IH) plays a pivotal role in the consequences of obstructive sleep apnea (OSA). It has been demonstrated that IH impairs nasomaxillary complex growth to reduce nasal airway cavity size in rodent models. Although turbinate dysfunction with inflammatory mucosal hypertrophy is related to OSA, the role of IH in turbinate hypertrophy with inflammation-driven fibrosis is unknown. Here, we aimed to clarify the pathogenesis of inflammatory mucosal hypertrophy and epithelial-mesenchymal transition (EMT) in the nasal turbinate under IH. Methods Seven-week-old male Sprague-Dawley rats were exposed to IH (4% O(2)to 21% O(2)with 0% CO2) at a rate of 20 cycles/h. Results Hypertrophy of the turbinate mucosa occurred after 3 weeks, with the turbinate mucosa of the experimental group becoming significantly thicker than in the control group. Immunostaining showed that IH increased the expression of TGF beta and N-cadherin and decreased E-cadherin expression in the turbinate mucosa. Quantitative PCR analysis demonstrated that IH enhanced the expression of not only the inflammatory markersTnf-a,Il-1b, andNos2but also the EMT markersTgf-b1,Col1a1, andPostn. Conclusions Collectively, these results suggest that IH induced turbinate hypertrophy via upregulation of gene expression related to inflammation and EMT in the nasal mucosa.

Automated summary

Chronic intermittent hypoxia (IH) in rats leads to hypertrophy of the turbinate mucosa, significantly increasing thickness. IH upregulates the expression of TGF beta and N-cadherin while downregulating E-cadherin. IH also enhances the expression of inflammatory and EMT markers in nasal mucosa, suggesting a role in inflammation and EMT-driven turbinate hypertrophy.