无鼻息肉病的慢性鼻窦炎患者基因表达与鼻窦炎症的地理分布

Amarbir S. Gill, J. Alt, A. Pulsipher, Kristine A. Smith, Nithya Subrahmanyam, Jorgen S. Sumsion, Joseph Jacob, B. Milash, R. Orlandi
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引用次数: 1

摘要

以正反馈的方式促进炎症,进一步增强CRS中其他1型炎症相关细胞因子的产生。越来越多的证据表明鼻腔内存在特定部位的基因表达模式。Platt等人研究了鼻腔内5个区域粘膜亚区鼻息肉中先前显示有差异表达的5个基因的表达水平,包括鼻外壁、鼻甲中部、下鼻甲、鼻中隔和鼻窦炎;作者发现,被分析者的基因表达模式存在显著差异。有趣的是,区域表达差异也可能与疾病负担和结果有关。Weibman等人证明,在钩突和鼻息肉组织之间测量的嗜酸性粒细胞区域表达差异在预测伴有鼻息肉的CRS患者的疾病负担和治疗结果方面具有实用价值。我们的数据表明,筛前窦和鼻底之间存在较大的局部基因表达差异。未来的研究应寻求比较鼻子内所有亚位点的基因表达和组织生物标志物,并包括一个非CRS对照队列,以了解CRS对所研究的基因表达差异的真正贡献。尽管我们确保所有入组的患者已停用口服类固醇2周,但有可能在这段时间结束时,他们的炎症状况没有恢复到基线。最后,合并症,如哮喘和过敏,包括过敏性鼻炎,可能会混淆我们在鼻窦局部识别的标志物。未来的研究应包括前瞻性活检收集和基因谱分析,增加伴有或不伴有哮喘和/或过敏的crsssnp患者的样本量,从而可以适当评估全身性炎症的潜在贡献。
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Topographic distribution of gene expression and sinonasal inflammation in chronic rhinosinusitis without nasal polyposis
promotes inflammation in a positive-feedback manner to further enhance the production of other type 1 inflammation- associated cytokines in CRS. 5 Increasing evidence suggests site- specific gene expression patterns within the sinonasal cavity. Platt et al. examined the ex pression level of five genes previously shown to be differentially expressed in nasal polyps in five regional mucosal subsites within the sinonasal cavity, including the lateral nasal wall, middle turbi -nate, inferior turbinate, septum and ethmoids; the authors found gene expression patterns of those analysed to differ significantly. 6 Interestingly, regional expression differences may also associate with disease burden and outcomes. Weibman et al. demonstrated that eosinophil regional expression differences measured between the uncinate process and nasal polyp tissue had utility in predicting both disease burden and outcome of treatment in patients with CRS with nasal polyps. 7 Our data suggest that large locoregional gene expression differences exist between the anterior ethmoid sinuses and the nasal floor. Future investigations should seek to compare gene expression and tissue biomarkers across all subsites within the nose and include a non- CRS control cohort in order to understand the true contribution of CRS to the gene expression differences ob -served. Although we ensured that all patients enrolled had been off oral steroids for 2 weeks, it is possible that their inflammatory profile had not returned to baseline by the end of this timeframe. Finally, comorbidities such as asthma and allergy, including allergic rhinitis, could confound the markers that we have identified locally in the sinuses. Future studies should include prospective biopsy collec tion and gene profiling with increased sample sizes of patients with CRSsNP with and without comorbid asthma and/or allergy, whereby the potential contribution of systemic inflammation can be properly assessed.
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