Scholarlink

<p>Epithelial-mesenchymal transition (EMT) can occur in chronic rhinosinusitis with nasal polyps (CRSwNP), and various cytokines are known to promote EMT profiles. However, the specific relationship between interleukin (IL)-17&#xa0;A and EMT in human nasal epithelial cells (hNECs) has not been previously clarified, highlighting a gap in understanding the mechanisms driving CRSwNP pathogenesis. In this study, the expression of IL-17&#xa0;A, NLR family pyrin domain containing 3 (NLRP3), transforming growth factor (TGF)-β1, and EMT-related genes was detected in nasal polyps from CRSwNP patients and control nasal tissues using immunohistochemistry, real-time polymerase chain reaction (PCR), and western blot. The results showed elevated levels of IL-17&#xa0;A, NLRP3, TGF-β1, and mesenchymal markers (vimentin and α-SMA), along with diminished E-cadherin expression in CRSwNP patients. In vitro experiments on hNECs revealed that IL-17&#xa0;A induced a dose-dependent up-regulation of vimentin, α-SMA, NLRP3, and TGF-β1, while down-regulating E-cadherin. Inhibition of the TGF-β1 signaling pathway effectively blocked EMT progression. Additionally, an NLRP3 inhibitor not only reduced IL-17&#xa0;A-induced NLRP3 expression but also suppressed TGF-β1 production and reversed the EMT phenotype. These findings suggest that IL-17&#xa0;A-induced EMT-like marker changes in hNECs are associated with increased NLRP3 and TGF-β1 signaling. Pharmacological inhibition of NLRP3 or TGF-β1 signaling partially attenuated these changes, suggesting that NLRP3 and TGF-β1 may participate in IL-17&#xa0;A-related epithelial remodeling in CRSwNP.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

NLRP3 participates in IL-17 A-induced epithelial-mesenchymal transition in human nasal epithelial cells of chronic rhinosinusitis with nasal polyps

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月25日

查看全文
  • Ying Zhang,
  • Xiaoyan Huang,
  • Zhipeng Zhang,
  • Jieqing Yu,
  • Qing Luo,
  • Jing Ye,
  • Danqing Yan

摘要

Epithelial-mesenchymal transition (EMT) can occur in chronic rhinosinusitis with nasal polyps (CRSwNP), and various cytokines are known to promote EMT profiles. However, the specific relationship between interleukin (IL)-17 A and EMT in human nasal epithelial cells (hNECs) has not been previously clarified, highlighting a gap in understanding the mechanisms driving CRSwNP pathogenesis. In this study, the expression of IL-17 A, NLR family pyrin domain containing 3 (NLRP3), transforming growth factor (TGF)-β1, and EMT-related genes was detected in nasal polyps from CRSwNP patients and control nasal tissues using immunohistochemistry, real-time polymerase chain reaction (PCR), and western blot. The results showed elevated levels of IL-17 A, NLRP3, TGF-β1, and mesenchymal markers (vimentin and α-SMA), along with diminished E-cadherin expression in CRSwNP patients. In vitro experiments on hNECs revealed that IL-17 A induced a dose-dependent up-regulation of vimentin, α-SMA, NLRP3, and TGF-β1, while down-regulating E-cadherin. Inhibition of the TGF-β1 signaling pathway effectively blocked EMT progression. Additionally, an NLRP3 inhibitor not only reduced IL-17 A-induced NLRP3 expression but also suppressed TGF-β1 production and reversed the EMT phenotype. These findings suggest that IL-17 A-induced EMT-like marker changes in hNECs are associated with increased NLRP3 and TGF-β1 signaling. Pharmacological inhibition of NLRP3 or TGF-β1 signaling partially attenuated these changes, suggesting that NLRP3 and TGF-β1 may participate in IL-17 A-related epithelial remodeling in CRSwNP.