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To cite this article: van den Berge M, ten Hacken NHT, van der Wiel E, Postma DS. Treatment of the bronchial tree from beginning to end: targeting small airway inflammation in asthma. Allergy 2013; 68: 16-26.

Small and large airway dysfunction poorly associate with asthma symptoms in our patients. However, deteriorations in small airway dysfunction are strongly related to an increase in dyspnea during bronchial provocation with methacholine. Small airway dysfunction contributes also independently to the clinical expression of asthma, as reflected by the severity of BHR.

BackgroundNasal gene expression profiling is a promising method to characterize COPD non-invasively. We aimed to identify a nasal gene expression profile to distinguish COPD patients from healthy controls. We investigated whether this COPD-associated gene expression profile in nasal epithelium is comparable with the profile observed in bronchial epithelium.MethodsGenome wide gene expression analysis was performed on nasal epithelial brushes of 31 severe COPD patients and 22 controls, all current smokers, using Affymetrix Human Gene 1.0 ST Arrays. We repeated the gene expression analysis on bronchial epithelial brushes in 2 independent cohorts of mild-to-moderate COPD patients and controls.ResultsIn nasal epithelium, 135 genes were significantly differentially expressed between severe COPD patients and controls, 21 being up- and 114 downregulated in COPD (false discovery rate < 0.01). Gene Set Enrichment Analysis (GSEA) showed significant concordant enrichment of COPD-associated nasal and bronchial gene expression in both independent cohorts (FDRGSEA < 0.001).ConclusionWe identified a nasal gene expression profile that differentiates severe COPD patients from controls. Of interest, part of the nasal gene expression changes in COPD mimics differentially expressed genes in the bronchus. These findings indicate that nasal gene expression profiling is potentially useful as a non-invasive biomarker in COPD.Trial registration ClinicalTrials.gov registration number NCT01351792 (registration date May 10, 2011), ClinicalTrials.gov registration number NCT00848406 (registration date February 19, 2009), ClinicalTrials.gov registration number NCT00807469 (registration date December 11, 2008).Electronic supplementary materialThe online version of this article (10.1186/s12931-017-0696-5) contains supplementary material, which is available to authorized users.

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Subjects with asymptomatic BHR may experience fewer symptoms in daily life because they have less small airway dysfunction.

BackgroundSmall airways dysfunction (SAD) contributes to the clinical expression of asthma. The identification of patients who suffer from SAD is important from a clinical perspective, as targeted therapy may improve patients’ well-being and treatment efficacy.AimsWe aimed to realize the first step in the development of a simple small airways dysfunction tool (SADT) that may help to identify asthma patients having SAD.MethodsAsthma patients with and without SAD were interviewed. Patients were selected to participate in this study based on FEF50% and R5-R20 values from spirometry and impulse oscillometry respectively.ResultsTen in depth interviews and two focus groups revealed that patients with and without SAD perceived differences in symptoms and signs, habits and health related issues. For example, patients with SAD reported to wheeze easily, were unable to breathe in deeply, mentioned more symptoms related to bronchial hyperresponsiveness, experienced more pronounced exercise-induced symptoms and more frequently had allergic respiratory symptoms after exposure to cats and birds. Based on these differences, 63 items were retained to be further explored for the SADT.ConclusionsThe first step of the development of the SADT tool shows that there are relevant differences in signs and respiratory symptoms between asthma patients with and without SAD. The next step is to test and validate all items in order to retain the most relevant items to create a short and simple tool, which should be useful to identify asthma patients with SAD in clinical practice.Electronic supplementary materialThe online version of this article (doi:10.1186/s12955-014-0155-7) contains supplementary material, which is available to authorized users.

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