Interleukin‐17A potentiates interleukin‐13‒induced eotaxin‐3 production by human nasal epithelial cells from patients with allergic rhinitis

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
出处
期刊:International Forum of Allergy & Rhinology [Wiley]
卷期号:9 (11): 1327-1333 被引量:9
标识
DOI:10.1002/alr.22382
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.
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