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首页> 外文期刊>Allergy >Role of muscarinic receptor activation in regulating immune cell activity in nasal mucosa.
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Role of muscarinic receptor activation in regulating immune cell activity in nasal mucosa.

机译:毒蕈碱受体激活在调节鼻黏膜免疫细胞活性中的作用。

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摘要

BACKGROUND: The prevalence of airway inflammatory disorders keeps rising; its pathogenic mechanism is still not fully understood. OBJECTIVE: The present study aimed to investigate the role of muscarinic receptor (M receptor) in regulating the immune cell activity in nasal mucosa by using surgical removed nasal mucosa from patients with nasal polyposis (NP) as a study platform. Methods: Human nasal mucosal sample was collected from inferior turbinectomy of 86 patients with NP or/and allergic rhinitis. Expression of tumor necrosis factor alpha (TNF-alpha), M receptor, OX40 ligand was measured in nasal mucosa by enzyme-linked immunosorbent assay, flow cytometry, and Western blotting assay. RESULTS: When compared with non-NP (nNP) nasal mucosa, contents of TNF-alpha and TNF-alpha+ cells markedly increased in NP nasal mucosa; immune staining colocalized M3 receptor+ and TNF-alpha+ cells in NP nasal mucosa; exposure of isolated CD4+ T cells to methacholine induced the release of TNF-alpha. We also found CD11c+/M3 receptor+ cells in NP nasal mucosa. Methacholine increased the expression of OX40L in dendritic cells. Staphylococcal (S) aureus and S. enterotoxin B (SEB) were detected in NP nasal mucosa. Exposure of dendritic cells or naive CD4+ T cells to SEB initiated the expression of M3 receptor at mRNA and protein levels. CONCLUSIONS: The present data demonstrate that parasympathetic activity has the capacity to activate dendritic cells to release OX40 ligand, the latter induces CD4+ T cells to produce IL-4 and TNF-alpha that may further contribute to the pathogenesis of NP.
机译:背景:气道炎性疾病的患病率持续上升。其致病机制仍不完全清楚。目的:以鼻息肉病(NP)患者手术切除的鼻黏膜为研究平台,探讨毒蕈碱受体(M受体)在调节鼻黏膜免疫细胞活性中的作用。方法:从86例NP或/和过敏性鼻炎患者的下鼻甲切除术中收集人鼻粘膜样品。通过酶联免疫吸附测定,流式细胞术和Western印迹测定法测量鼻粘膜中肿瘤坏死因子α(TNF-α),M受体,OX40配体的表达。结果:与非NP鼻腔黏膜相比,NP鼻腔黏膜中TNF-α和TNF-α+细胞的含量明显增加。免疫染色NP鼻黏膜中的M3受体+和TNF-α+细胞共定位;将分离的CD4 + T细胞暴露于乙酰甲胆碱可诱导TNF-α的释放。我们还在NP鼻粘膜中发现了CD11c + / M3受体+细胞。甲胆碱可提高树突状细胞中OX40L的表达。在NP鼻粘膜中检测到葡萄球菌(S)金黄色葡萄球菌和肠毒素B(SEB)。将树突状细胞或幼稚的CD4 + T细胞暴露于SEB会启动M3受体在mRNA和蛋白水平上的表达。结论:本数据表明副交感神经具有激活树突状细胞释放OX40配体的能力,后者诱导CD4 + T细胞产生IL-4和TNF-α,可能进一步促进NP的发病。

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