嗜酸性粒细胞趋化因子
STAT6
白细胞介素13
医学
免疫学
细胞因子
白细胞介素
嗜酸性粒细胞
白细胞介素5
白细胞介素17
STAT蛋白
炎症
白细胞介素4
信号转导
趋化因子
车站3
生物
细胞生物学
哮喘
作者
Wei Wei Wang,Kai Zhu,Hong Yu,Yong Liang Pan
摘要
Background Interleukin (IL)‐17A is involved in the pathogenesis of allergic rhinitis (AR). Increased expression of IL‐17A is correlated with disease severity and nasal eosinophilia. However, the molecular mechanisms by which IL‐17A contributes to T‐helper 2 cytokine IL‐13‒driven pathology in AR remain unclear. We sought to obtain mechanistic insight into how IL‐17A and IL‐13 regulate the epithelial production of eotaxin‐3 representing eosinophilic inflammation in AR. Methods Human nasal epithelial cells (HNECs) from AR patients were cultured and stimulated with IL‐17A, IL‐13, or IL‐17A and IL‐13. Phosphorylated signal transducer activator of transcription 6 (p‐STAT6) and suppressor of cytokine signaling 1 (SOCS1) in HNECs were assayed using Western blotting. Immunocytochemistry was used to determine p‐STAT6‒positive expression in the cells. Eotaxin‐3 expression in the cells and culture supernatants was evaluated using real‐time polymerase chain reaction and enzyme‐linked immunosorbent assays. Results Stimulation with IL‐13 alone induced STAT6 phosphorylation and promoted p‐STAT6 nuclear translocation, leading to eotaxin‐3 production by HNECs. These effects were further enhanced by cotreatment with IL‐13 and IL‐17A, whereas IL‐17A alone had no impact on STAT6 or eotaxin‐3 expression. Incubation with IL‐17A or IL‐13 increased the level of SOCS1 protein in the cells, whereas the addition of IL‐17A attenuated IL‐13‒induced SOCS1 expression. Conclusion IL‐17A potentiated IL‐13‒driven STAT6 activation through the downregulation of SOCS1 expression, leading to enhancement of eotaxin‐3 production by HNECs. These factors contributed to eosinophilic inflammation in AR.
科研通智能强力驱动
Strongly Powered by AbleSci AI