Release of Type 2 Cytokines by Epithelial Cells of Nasal Polyps.
Release of Type 2 Cytokines by Epithelial Cells of Nasal Polyps.
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DOI：
10.1155/2016/2643297
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发表时间：
2016
影响因子：
4.1
通讯作者：
Rolla G
中科院分区：
文献类型：
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作者：
Boita M;Bucca C;Riva G;Heffler E;Rolla G
背景慢性鼻窦炎伴鼻息肉（CRSwNP）的T2炎症可能受上皮细胞因子释放（TSLP、IL-25和IL-33）的影响。我们研究了无鼻息肉的慢性鼻窦炎（CRSsNP）患者上皮CRSwNP细胞与上皮窦粘膜细胞释放TSLP、IL-25和IL-33的情况。方法.在基线条件下和用屋尘螨（DP）、烟曲霉（AF）和poly（I：C）刺激后，通过ELISA测量由CRSwNP（9名患者，6名特应性）和CRSsNP（7名患者，2名特应性）衍生的细胞培养物上清液中的IL-25、IL-33和TSLP。结果CRSwNP上皮细胞释放增加水平的IL-25（从0.12 ± 0.06 pg/ml到0.27 ± 0.1 pg/ml，p < 0.01）和TSLP（从0.77 ± 0.5 pg/ml到2.53 ± 1.17 pg/ml，p < 0.001），而CRSsNP上皮细胞在AF和DP刺激后分别释放增加水平的IL-25和IL-33，（IL-25：从0.18 ± 0.07 pg/ml至0.51 ± 0.1 pg/ml，p < 0.001; IL-33：从2.57 ± 1.3 pg/ml至5.7 ± 3.1 pg/ml，p < 0.001）。结论. CRSwNP上皮细胞释放TSLP和IL-25时，刺激聚（I：C），但不是DP或AF，表明病毒感染可能有助于维持和放大T2免疫反应中看到CRSwNP。
Background. T2 inflammation of chronic rhinosinusitis with nasal polyps (CRSwNP) may be influenced by epithelial cytokines release (TSLP, IL-25, and IL-33). We investigated the release of TSLP, IL-25, and IL-33 by epithelial CRSwNP cells compared to epithelial sinus mucosa cells of patients with chronic rhinosinusitis without nasal polyps (CRSsNP). Methods. IL-25, IL-33, and TSLP were measured by ELISA in the supernatant of cell cultures derived by CRSwNP (9 patients, 6 atopic) and CRSsNP (7 patients, 2 atopic) in baseline condition and following stimulation with Dermatophagoides pteronyssinus (DP), Aspergillus fumigatus (AF), and poly(I:C). Results. CRSwNP epithelial cells released increased levels of IL-25 (from 0.12 ± 0.06 pg/ml to 0.27 ± 0.1 pg/ml, p < 0.01) and TSLP (from 0.77 ± 0.5 pg/ml to 2.53 ± 1.17 pg/ml, p < 0.001) following poly(I:C) stimulation, while CRSsNP epithelial cells released increased levels of IL-25 and IL-33 following AF and DP stimulation, respectively (IL-25: from 0.18 ± 0.07 pg/ml to 0.51 ± 0.1 pg/ml, p < 0.001; IL-33: from 2.57 ± 1.3 pg/ml to 5.7 ± 3.1 pg/ml, p < 0.001). Conclusions. CRSwNP epithelial cells release TSLP and IL-25 when stimulated by poly(I:C) but not by DP or AF, suggesting that viral infection may contribute to maintain and amplify the T2 immune response seen in CRSwNP.