抽象的
OGP phenotype is not characterised by obstructive sleep apnoeahttp://bit.ly/2kv2cke
From the authors:
我们感谢C. Ward和Z.J.卡拉巴(Kharaba1]。
关于他们对使用A549细胞系的查询,尚未描述质子泵抑制剂(PPI)和胆汁酸对气道上皮转录组的影响。因此,为了估算PPI和胆汁酸对上皮失调的潜在影响,我们利用了从可自由访问的数据库获得的信息,列出了不同细胞系对超过27 000个遗传或化学性扰动的转录响应[2]。We chose to analyse the transcriptional responses of A459 lung epithelial cells to PPI and bile acids, as this was the most suitable cell line available in the database. Using these data, we identified high connectivity scores, suggesting a direct impact of bile acids and PPI on immune mechanisms in severe asthma. We agree that caution needs to be taken when interpreting data from the A549 cell line, which was established from a human lung carcinoma, and this is why we stated that our study should be viewed as exploratory. The hypotheses generated from this study are currently being tested in our laboratory, this time using primary bronchial epithelial cells cultured体外。
C. Ward and Z.J. Kharaba rightly highlight the potential for modification of the airway microbiome as a mechanism involved in epithelial dysregulation associated with severe asthma, gastro-oesophageal reflux disease (GORD) and obesity. GORD is, indeed, associated with changes in oesophageal microbiota [3]。Furthermore, Golevaet al.[4]最近描述链球菌species, includingS. mitis和S.伪内膜发现能够改变对皮质类固醇的上皮反应体外。尽管在U-Biopred研究的一部分参与者中分析了气道微生物组,但不幸的是,没有足够的参与者提供转录组和微生物组数据,因此我们无法将微生物组与Gord,肥胖和PPI治疗的影响相关联。
The complexity of severe asthma management includes co-morbidities such as obstructive sleep apnoea syndrome (OSAS), which has been associated with poor asthma control, increased burden of asthma independent of any association with obesity and increased hospitalisation length of stay after exacerbation [5]。The impact of OSAS treatment on asthma outcomes is unclear [6,7];该机制可能涉及核因子-κB依赖性促炎细胞因子的产生和缺氧因子1途径[8]。使用Epworth嗜睡评分(ESS)在U-Biopred研究中评估了OSA。我们的分析表明,OGP(肥胖,胃食管反流和质子泵抑制剂的使用)表型与严重的哮喘簇C2和C3没有差异,就总ESS评分而言(OGP 9.82±4.13)相对C2中的8.24±4.28,C3中的7.7±5.16)和ESS> 10的受试者数量(轻度过度的白天嗜睡; OGP 4/21,C2英寸5/23,C3中的7/22)。
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脚注
利益冲突:J-M。Perotin无话可说。
Conflict of interest: R. Djukanovic reports receiving fees for lectures at symposia organised by Novartis, AstraZeneca and TEVA, consultation for TEVA and Novartis as member of advisory boards, and participation in a scientific discussion about asthma organised by GlaxoSmithKline, and is a co-founder and current consultant, and has shares in Synairgen, a University of Southampton spin out company.
Conflict of interest: D.E. Davies has nothing to disclose.
Support statement: This work was supported by ARAIRCHAR (grant 2017); ANAFORCAL (grant: Bourse anaforcal 2017); European Respiratory Society (grant: ERS long term fellowship 2017). Funding information for this article has been deposited with theCrossref Funder Registry。
- 已收到2019年9月13日。
- Accepted2019年9月13日。
- 版权所有©ERS 2019