Molecular markers of type 2 airway inflammation do not differ between eosinophilic asthma and eosinophilic chronic obstructive pulmonary disease (COPD); however, the relationship between eosinophilia and type 2 airway markers appears weaker in COPD than in severe asthma, according to study results published in Allergy, the official journal of the European Academy of Allergy and Clinical Immunology.

Airway and systemic eosinophilia are treatable traits in both severe asthma and COPD; however, the molecular basis of eosinophilia in COPD is poorly understood and may involve type 2 cytokines (interleukin-5 [IL-5], interleukin-13 [IL-13]) and prostaglandin D2 (PGD2). Therefore, researchers sought to determine whether type 2 inflammatory pathways (sputum IL-5, IL-13, hematopoietic PGD2 synthase [HPGDS] gene expression, and PGD2 levels) differed between eosinophilic and noneosinophilic severe asthma and COPD. Researchers included 19 individuals without obstructive airway disease (control group), 96 individuals with COPD, and 84 individuals with severe asthma. The participants were categorized as eosinophilic using either sputum eosinophil (≥3%) or blood eosinophil count (≥300/µL).

Type 2 markers did not differ across groups except HPGDS mRNA, which was highest in individuals without obstructive airway disease and lowest in COPD. IL-5 and IL-13 mRNA and PGD2 levels were significantly higher in eosinophilic vs noneosinophilic severe asthma but did not differ between eosinophilic COPD and eosinophilic severe asthma or noneosinophilic COPD. HPGDS expression was higher in eosinophilic severe asthma compared with eosinophilic COPD. Results were similar using sputum or blood eosinophil cut-offs. Sputum IL-5 and IL-13 were highly correlated with each other in severe asthma (P <.001) and COPD (P <.001), moderately correlated with sputum eosinophils in severe asthma (P <.001), and weakly correlated, but statistically significant, in COPD (P <.05).

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“These data support the hypothesis that airway and systemic eosinophilic inflammation in COPD is promoted, at least in part, by mechanisms distinct to the canonical type 2 inflammatory pathway that is prominent in asthma,” the researchers concluded.

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.


Fricker M, McDonald VM, Winter NA, et al. Molecular markers of type 2 airway inflammation are similar between eosinophilic severe asthma and eosinophilic COPD. Allergy. Published online January 20, 2021. doi:10.1111/all.14741