In asthma, change is the only constant

Abstract

Variability is a hallmark of asthma, whether that be in morning and evening peak flow, the seasonality of exacerbations or responsiveness to treatment (1). The drivers of disease variation are manifold, but are particularly troublesome when it comes to the responsiveness to corticosteroid treatment, our mainstay of disease control. A lack of corticosteroid responsiveness is a characteristic of severe asthma (2), significantly impacting patients’ mortality and morbidity, particularly in relation to exacerbation frequency. The presence of eosinophils in blood or sputum are linked to a steroid-sensitive T2-driven inflammation and the presence of these cells are often used to guide the use of corticosteroids as well as biologic therapies (3). In contrast, sputum neutrophils are linked to activation of steroid-insensitive T1-pathways (4), but the drivers and stability of these pathways are not well understood. Further understanding of the mechanisms that lead to this corticosteroid resistance are therefore required to allow targeted treatment of these steroid unresponsive pathways to bring patient benefit. In this issue of the Journal, Fahy and colleagues provide insight into these disease mechanisms using RNA Sequencing data derived from the sputa of asthma patients in the SARP-3 study collected longitudinally (5). Additionally, sputa from a subcohort of patients was analysed following intramuscular injection of the corticosteroid, triamcinolone acetonide (TA).

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Identifiers

ORCID for Karl J. Staples: orcid.org/0000-0003-3844-6457

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