Identification of airway mucosal type 2 inflammation by using clinical biomarkers in asthmatic patients

Asthma is a complex disease of the airways characterized by inflammation and dynamic airway obstruction.  Despite the single, more recent evidence suggests that asthma is mediated by a set of distinct immune abnormalities.  In this month’s issue of JACI, Silkoff and colleagues report the results of the ADEPT (Airways Disease Endotyping for Personal Therapeutics) study, in which 83 patients with mild, moderate, and severe asthma as well as 25 healthy non-asthmatic subjects were examined for biomarkers of asthma (J Allergy Clin Immunol 2017; 140(3): 710-719).  They underwent bronchoscopy to obtain tissue samples, and then had the biomarkers measured in the lab to characterize them as having either high or low levels of type 2 inflammatory mediators.  These were then correlated with clinical variables.

They determined the presence of type 2 inflammation based on airway expression of CCL26, periostin, and IL-13 in vitro signature (IVS).  They then looked at the clinical variables, including fraction of exhaled nitric oxide (FENO) levels, blood eosinophil counts, serum CCL26 expression and serum CCL17 expression.  What they found was that the combination of Fractional Excretion of Nitric Oxide (FENO), blood eosinophil counts, serum CCL17 and serum CCL26 had a positive predictive value of 100% for patients determined to be in the asthma group driven by type 2 inflammation.  This is important because individual clinical characteristics alone could not predict the pattern of type 2 inflammatory markers, and eosinophilic inflammation was associated with , but not limited to, gene expression for type 2 inflammation in airways.

By describing a set of relatively easily obtainable clinical markers consistent with type 2 inflammation, the authors report information that can help researchers and practitioners tailor the most appropriate therapy for those with asthma mediated by type 2 inflammation.

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