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The molecular basis of eosinophilia in COPD is poorly understood but could involve type 2 cytokines (IL5, IL13) and prostaglandin D<jats:sub>2<\/jats:sub> (PGD<jats:sub>2<\/jats:sub>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This study included non\u2010obstructive airways disease (OAD) controls (<jats:italic>n<\/jats:italic>\u00a0=\u00a019), a COPD cohort (<jats:italic>n<\/jats:italic>\u00a0=\u00a096) and a severe asthma cohort (<jats:italic>n<\/jats:italic>\u00a0=\u00a084). Demographics, exacerbation history, disease impact (SGRQ) and spirometry were assessed. Participants were categorized as eosinophilic using either sputum eosinophil proportion (\u22653%) or blood eosinophil count (\u2265300\/\u03bcL). Sputum type 2 inflammatory measures included PGD<jats:sub>2<\/jats:sub> by ELISA and gene expression (qPCR) of <jats:italic>IL5<\/jats:italic>, <jats:italic>IL13<\/jats:italic> and the haematopoietic PGD<jats:sub>2<\/jats:sub> synthase (<jats:italic>HPGDS<\/jats:italic>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Type 2 markers did not differ across groups except <jats:italic>HPGDS<\/jats:italic> mRNA which was highest in non\u2010OAD controls and lowest in COPD. <jats:italic>IL5<\/jats:italic> and <jats:italic>IL13<\/jats:italic> mRNA and PGD<jats:sub>2<\/jats:sub> levels were significantly increased in eosinophilic vs non\u2010eosinophilic severe asthma but did not differ between eosinophilic COPD and eosinophilic severe asthma or non\u2010eosinophilic COPD. <jats:italic>HPGDS<\/jats:italic> expression was higher in eosinophilic severe asthma compared with eosinophilic COPD. Results were similar using sputum or blood eosinophil cut\u2010offs. Sputum <jats:italic>IL5<\/jats:italic> and <jats:italic>IL13<\/jats:italic> were highly intercorrelated in severe asthma (<jats:italic>r<\/jats:italic>\u00a0=\u00a00.907, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.001) and COPD (<jats:italic>r<\/jats:italic>\u00a0=\u00a00.824, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.001), were moderately correlated with sputum eosinophils in severe asthma (<jats:italic>IL5<\/jats:italic> <jats:italic>r<\/jats:italic>\u00a0=\u00a00.440, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.001; <jats:italic>IL13<\/jats:italic> <jats:italic>r<\/jats:italic>\u00a0=\u00a00.428, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.001) and were weakly correlated in COPD (<jats:italic>IL5<\/jats:italic> <jats:italic>r<\/jats:italic>\u00a0=\u00a00.245, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05; <jats:italic>IL13<\/jats:italic> <jats:italic>r<\/jats:italic>\u00a0=\u00a00.317, <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Molecular markers of type 2 airway inflammation do not differ between eosinophilic asthma and eosinophilic COPD; however, the relationship between eosinophilia and type 2 airway markers appears weaker in COPD than in severe asthma.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.14741","type":"journal-article","created":{"date-parts":[[2021,1,20]],"date-time":"2021-01-20T14:52:36Z","timestamp":1611154356000},"page":"2079-2089","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Molecular markers of type 2 airway inflammation are similar between eosinophilic severe asthma and eosinophilic chronic obstructive pulmonary disease"],"prefix":"10.1111","volume":"76","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8587-1774","authenticated-orcid":false,"given":"Michael","family":"Fricker","sequence":"first","affiliation":[{"name":"School of Medicine and Public Health Faculty of Health and Medicine and Priority Research Centre for Healthy Lungs The University of Newcastle Callaghan NSW Australia"},{"name":"National Health and Medical Research Council Centre for Excellence in Severe Asthma Newcastle NSW Australia"},{"name":"Hunter Medical Research Institute Newcastle NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanessa M.","family":"McDonald","sequence":"additional","affiliation":[{"name":"National Health and Medical Research Council Centre for Excellence in Severe Asthma Newcastle NSW Australia"},{"name":"Hunter Medical Research Institute Newcastle NSW Australia"},{"name":"School of Nursing and Midwifery Faculty of Health and Medicine and Priority Research Centre for Healthy Lungs The University of Newcastle Callaghan NSW Australia"},{"name":"Department of Respiratory and Sleep Medicine John Hunter Hospital Newcastle NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha A.","family":"Winter","sequence":"additional","affiliation":[{"name":"School of Medicine and Public Health Faculty of Health and Medicine and Priority Research Centre for Healthy Lungs The University of Newcastle Callaghan NSW Australia"},{"name":"National Health and Medical Research Council Centre for Excellence in Severe Asthma Newcastle NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine J.","family":"Baines","sequence":"additional","affiliation":[{"name":"School of Medicine and Public Health Faculty of Health and Medicine and Priority Research Centre for Healthy Lungs The University of Newcastle Callaghan NSW Australia"},{"name":"Hunter Medical Research Institute Newcastle NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter A. 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