Human asthma phenotypes: from the clinic, to cytokines, and back again.
Human asthma phenotypes: from the clinic, to cytokines, and back again.
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DOI：
10.1111/j.1600-065x.2011.01032.x
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发表时间：
2011-07
影响因子：
8.7
通讯作者：
Woodruff PG
中科院分区：
文献类型：
--
作者：
Bhakta NR;Woodruff PG
大量实验证据支持t -辅助性2 （Th2）细胞因子在动物模型中协调过敏性气道炎症的假设。然而，人类哮喘在临床特征、炎症的细胞来源和对常见治疗的反应方面是异质性的。使用痰细胞学以及使用细胞和临床数据的无偏聚类方法研究了这种疾病的异质性。细胞因子驱动炎症的重要差异可能是这种异质性的基础，对人类哮喘患者的研究已经开始阐明这些分子差异。这种分子异质性可以通过现有的生物标志物（诱导痰评估或呼出一氧化氮测试）来评估，也可能需要新的生物标志物。针对Th2细胞因子的新兴疗法的有效测试和应用将取决于哮喘中这种分子异质性的准确和容易获得的生物标志物。此外，是否其他非th2细胞因子通路是哮喘患者特定亚群气道炎症的基础，这是一个未解决的问题，也是未来使用小鼠模型和人体研究的重要目标。
A large body of experimental evidence supports the hypothesis that T-helper 2 (Th2) cytokines orchestrate allergic airway inflammation in animal models. However, human asthma is heterogeneous with respect to clinical features, cellular sources of inflammation, and response to common therapies. This disease heterogeneity has been investigated using sputum cytology as well as unbiased clustering approaches using cellular and clinical data. Important differences in cytokine-driven inflammation may underlie this heterogeneity, and studies in human subjects with asthma have begun to elucidate these molecular differences. This molecular heterogeneity may be assessed by existing biomarkers (induced sputum evaluation or exhaled nitric oxide testing) or may require novel biomarkers. Effective testing and application of emerging therapies that target Th2 cytokines will depend on accurate and easily obtained biomarkers of this molecular heterogeneity in asthma. Furthermore, whether other non-Th2 cytokine pathways underlie airway inflammation in specific subsets of patients with asthma is an unresolved question and an important goal of future research using both mouse models and human studies.