Abstract
AbstractAntrochoanal polyp (ACP) is a benign nasal mass of unknown etiology. Tight junctions (TJs) are essential to the epithelial barrier that protects the body from external damage. The samples were collected from 49 controls, 37 patients with ACP and 45 patients with nasal polyp (NP). qRT-PCR and immunofluorescence staining were performed to analyze the expressions of TJs markers (ZO-1, Claudin-3 and Occludin) and ZEB1. The expression levels of TJs markers were analyzed in primary human nasal epithelial cells (hNECs) transfected with IL-17A and ZEB1 small interfering RNA (si-ZEB1). The levels of ZO-1 and Occludin mRNA were significantly downregulated in the ACP compared with the control and NP groups, and the expression of Claudin-3 was markedly lower in the ACP than control group. Immunofluorescence staining showed that the staining intensity of TJs markers was significantly decreased in the ACP and NP groups, and there was no difference between NP and ACP groups. Meanwhile, ZEB1 expression was significantly upregulated in ACP group. In hNECs, The IL-17A group showed much weaker expression of ZO-1, Claudin3 and Occludin compared to the control group.IL-17A and si-ZEB1 group reversed the down-regulation of the expression of TJs-related molecules. In addition, we observed that the degree of disruption of tight junctions correlated with the severity of the disease. The tight junctions in the ACP were extremely damaged and were correlated with the severity of the disease. In conclusion, ZEB1 was involved in the pathogenesis of ACP mediated by IL-17A though regulating tight junctions.
Publisher
Research Square Platform LLC