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To the Editor, Type 2 (T2) inflammation in asthma encompasses the presence of eosinophilic inflammation and/or selected cytokines including interleukin (IL)-13. Some chronic obstructive pulmonary disease (COPD) patients have increased airway eosinophil numbers,1 which is associated with greater effects of inhaled corticosteroids (ICS).2 Studies of T2 inflammation in COPD have used hypothesis free, open platform approaches.3, 4 We used these results, plus data from T2 asthma studies,5 to test a restricted panel of biomarkers (chloride channel accessory 1 [CLCA1], periostin [POSTN], serpin family B member 2 [SERPINB2], C-C motif chemokine ligand 26 [CCL26], IL-13 and cystatin SN [CST1]) to further investigate the nature of T2 inflammation in eosinophilic COPD. We used two cohorts: bronchial brushings and sputum were obtained from 17 eosinophilhigh and 20 eosinophillow COPD patients (bronchoscopy cohort previously reported1: eosinophilhigh defined as blood eosinophils > 250 eosinophils µL−1 and eosinophillow defined as blood eosinophils < 150 eosinophils µL−1) and sputum only was obtained from 15 eosinophilhigh and 18 eosinophillow COPD patients (validation cohort: eosinophilhigh defined as > 150 eosinophils µL−1 blood and > 3% sputum eosinophils and eosinophillow defined as < 150 eosinophils µL−1 blood and < 3% sputum eosinophils). Full details of inclusion criteria and clinical characteristics are in the Appendix S1 and Table 1. Both cohorts were generally well matched. RNA sequencing examined gene expression in the bronchoscopy cohort, while RT-qPCR was used in the validation cohort. Full details of methods and analysis are in the Appendix S1. In the bronchoscopy cohort, bronchial epithelial gene expression of CLCA1, CCL26, IL-13 and CST1 was significantly higher (P < .05) in eosinophilhigh versus eosinophillow COPD patients (Figure 1) with fold change differences of 1.9, 2.2, 2.9 and 2.5, respectively. POSTN and SERPINB2 expression trended higher in eosinophilhigh versus eosinophillow COPD patients but did not achieve statistical significance (P = .06 and P = .07, respectively; Figure S1). In the bronchoscopy and validation cohorts, sputum gene expression of CLCA1, CCL26, IL-13 and CST1 was significantly higher (P < .05) in eosinophilhigh versus eosinophillow COPD patients (Figure 1); fold change differences were 3.1, 2.0, 1.8 and 3.5 for the bronchoscopy cohort and 28.2, 9.4, 6.0 and 79.3 for the validation cohort, respectively. Expression of POSTN and SERPINB2 was not different between groups (Figure S1). ICS use and smoking status did not influence gene expression (data not shown). There was a significant positive correlation between a four-gene mean and sputum eosinophil counts in both cohorts (rho 0.6 to 0.7 and P < .001; Figure S1), but not other cell types (data not shown). We report that eosinophilic COPD is associated with a profile of T2 inflammation in both bronchial epithelium and sputum samples; this was consistently observed in sputum samples from two independent cohorts. We tested six genes associated with T2 inflammation in asthma and observed increased expression of four of these genes (CLCA1, CCL26, IL-13 and CST1) in eosinophilhigh compared to eosinophillow COPD patients. The strengths of this study include a validation cohort, and different lung samples (bronchial epithelium and sputum). The positive signals were > 1.8-fold higher (gene expression) in the eosinophilhigh group. Different techniques (RNA sequencing and RT-qPCR) were used to analyse sputum samples, but the conclusions and relative fold changes showed the same pattern, adding confidence to our observations. The association between eosinophils and IL-13 expression levels suggests pathways linking eosinophilic inflammation to airway remodelling and mucus secretion,6 discussed further in the Appendix S1. These results indicate a wider profile of T2 inflammation in eosinophilic COPD that extends to mechanisms including IL-13 driven pathways. While T2 inflammation is well recognized in asthma, we now provide further evidence of T2 inflammation in a subset of COPD patients. The components of T2 inflammation described here may represent therapeutic targets. This research was co-funded by the NIHR Manchester Biomedical Research Centre and the North West Lung Centre Charity, Manchester. This report is independent research, and the views expressed in this publication are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Data included in this study were obtained from samples collected from a previous bronchoscopy study funded by Medimmune. AH has received personal fees from Chiesi. AB, SW, NJ, GL, UK and TS have no conflicts of interest. T-HP, SS, CM and PN are employees of AstraZeneca. DS has received personal fess from AstraZeneca, Boehringer Ingelheim, Chiesi, Cipla, GlaxoSmithKline, Glenmark, Menarini, Mundipharma, Novartis, Peptinnovate, Pfizer, Pulmatrix, Therevance and Verona. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.