# paper.pdf ## Metadata - PDFFormatVersion=1.4 - IsLinearized=false - IsAcroFormPresent=false - IsXFAPresent=false - IsCollectionPresent=false - IsSignaturesPresent=false - Custom.CrossmarkMajorVersionDate=2014-12-12 - Custom.CrossmarkDomainExclusive=false - Custom.doi=10.1183/23120541.01397-2025 - Custom.CrossMarkDomains[1]=psychoceramics.labs.crossref.org - CreationDate=D:20260701135749+05'30' - Author=Michal Shteinberg - Creator=Arbortext Advanced Print Publisher 10.0.1465/W Unicode - Producer=Acrobat Distiller 8.1.0 (Windows) - ModDate=D:20260711065216+05'30' - Title=The association between chronic rhinosinusitis, bronchiectasis and type 2 inflammation: an EMBARC registry analysis - xap:createdate=2026-07-01T13:57:49+05:30 - xap:creatortool=Arbortext Advanced Print Publisher 10.0.1465/W Unicode - xap:modifydate=2026-07-11T06:52:16+05:30 - xap:metadatadate=2026-07-11T06:52:16+05:30 - pdf:producer=Acrobat Distiller 8.1.0 (Windows) - dc:format=application/pdf - dc:identifier=10.1183/23120541.01397-2025 - dc:title=The association between chronic rhinosinusitis, bronchiectasis and type 2 inflammation: an EMBARC registry analysis - dc:creator=Michal Shteinberg,Charles S. Haworth,Jennifer Pollock,Shai Cohen,Michael R. Loebinger,Jenny Jrbashyan,Katerina Dimakou,Nizar Abo Helo,Stefano Aliberti,Nili Stein,Felix C. Ringshausen,Yochai Adir,Anthony De Soyza,Montserrat Vendrell,Pierre Régis Burgel,Oriol Sibila,Apostolos Bossios,Holly Lind,Kateryna Viligorska,Kara Robertson,Paula Kauppi,Branislava Milenkovic,Rosario Menendez,Oxana Munteanu,Dusanka Obradovic,Adam Nowinski,Adelina Amorim,Antoni Torres,Natalie Lorent,Eva Van Braeckel,Muhammad Anwar,Salvatore Battalglia,Amelia Shoemark,Wim Boersma,Pieter C. Goeminne,Francesco Blasi,Eva Polverino,James D. Chalmers - xapmm:documentid=uuid:6ea38ac4-ea3b-477f-a923-8df6173a920b - xapmm:instanceid=uuid:9ff58ca2-be0b-40f8-9987-8e2947792388 - prism:url=http://dx.doi.org/10.1183/23120541.01397-2025 - prism:doi=10.1183/23120541.01397-2025 - crossmark:doi=10.1183/23120541.01397-2025 - crossmark:crossmarkdomainexclusive=false - crossmark:majorversiondate=2014-12-12 - crossmark:crossmarkdomains=psychoceramics.labs.crossref.org - pdfx:crossmarkdomainexclusive=false - pdfx:crossmarkmajorversiondate=2014-12-12 - pdfx:doi=10.1183/23120541.01397-2025 - pdfx:crossmarkdomains=psychoceramics.labs.crossref.org ## Contents ### Page 1 The association between chronic rhinosinusitis, bronchiectasis and type 2 inflammation: an EMBARC registry analysis Michal Shteinberg , Charles S. Haworth, Jennifer Pollock, Shai Cohen, Michael R. Loebinger, Jenny Jrbashyan, Katerina Dimakou, Nizar Abo Helo, Stefano Aliberti , Nili Stein, Felix C. Ringshausen , Yochai Adir, Anthony De Soyza , Montserrat Vendrell, Pierre Régis Burgel , Oriol Sibila, Apostolos Bossios , Holly Lind, Kateryna Viligorska, Kara Robertson, Paula Kauppi, Branislava Milenkovic, Rosario Menendez, Oxana Munteanu, Dusanka Obradovic, Adam Nowinski, Adelina Amorim, Antoni Torres , Natalie Lorent , Eva Van Braeckel , Muhammad Anwar, Salvatore Battalglia , Amelia Shoemark , Wim Boersma, Pieter C. Goeminne, Francesco Blasi, Eva Polverino and James D. Chalmers on behalf of the EMBARC registry investigatorsThe association between chronic rhinosinusitis, bronchiectasis and type 2 inflammation: an EMBARC registry analysis16 640 individuals with bronchiectasis Stratified by CRS status EMBARCThe European Bronchiectasis Registry No CRS: 12 714 • Chronic rhinosinusitis with (CRSwNP) and without nasal polyps (CRSnNP) are prevalent in bronchiectasis • GREATER symptom burden and more bacterial infection in bronchiectasis with concomitant CRSnNP and CRSwNP • LESS mortality and hospitalisations with concomitant CRSnNP and CRSwNP • CRSwNP, male sex, asthma and ABPA are independent predictors of type 2 inflammation CRSnNP: 2703 CRSwNP: 1223 60.0 Airway pathogen isolation No CRS (n=12 714) CRS without nasal polyps (n=2703) CRS with nasal polyps (n=1223) 50.0 40.0 30.0 20.0 10.0 0.0 Any bacterial colonisation Frequency (%)Pseudomonas aeruginosa Hemophilus influenzae Moraxella catarrhalisEnterobacteriaceaeStaphylococcus aureus Streptococcus pneumoniae Stenotrophomonas sp.AspergillusGRAPHICAL ABSTRACT Overview of the study. CRS: chronic rhinosinusitis; ABPA: allergic bronchopulmonary aspergillosis. https://doi.org/10.1183/23120541.01397-2025 ERJ Open Res 2026; 12: 01397-2025ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE M. SHTEINBERG ET AL. ### Page 2 The association between chronic rhinosinusitis, bronchiectasis and type 2 inflammation: an EMBARC registry analysis Michal Shteinberg 1,2, Charles S. Haworth3, Jennifer Pollock4, Shai Cohen2,5, Michael R. Loebinger6, Jenny Jrbashyan7, Katerina Dimakou8, Nizar Abo Helo5, Stefano Aliberti 9, Nili Stein10, Felix C. Ringshausen 11,12,13, Yochai Adir1,2, Anthony De Soyza 14, Montserrat Vendrell15, Pierre Régis Burgel 16, Oriol Sibila17, Apostolos Bossios 18, Holly Lind4, Kateryna Viligorska4, Kara Robertson4, Paula Kauppi19, Branislava Milenkovic20, Rosario Menendez21, Oxana Munteanu22, Dusanka Obradovic23,24, Adam Nowinski25, Adelina Amorim26, Antoni Torres 27, Natalie Lorent 28, Eva Van Braeckel 29, Muhammad Anwar30, Salvatore Battalglia 31, Amelia Shoemark 4, Wim Boersma32, Pieter C. Goeminne33, Francesco Blasi34,35, Eva Polverino27 and James D. Chalmers4 on behalf of the EMBARC registry investigators1Pulmonology Institute, Carmel Medical Center, Haifa, Israel. 2The B. Rappaport Faculty of Medicine, The Technion – Israel Institute of Technology, Haifa, Israel. 3Royal Papworth Hospital and University of Cambridge, Cambridge, UK. 4Division of Respiratory Medicine and Gastroenterology, University of Dundee, Dundee, UK. 5Immunology and Internal Medicine B, Carmel Medical Center, Haifa, Israel. 6Royal Brompton and Harefield Hospitals, Imperial College London, London, UK. 7Otolaryngology Department, Carmel Medical Center, Haifa, Israel. 8General Hospital for Chest Diseases of Athens Sotiria, Athens, Greece. 9IRCCS Humanitas Research Hospital and Humanitas University, Milan, Italy. 10Department of Epidemiology and Community Medicine, Carmel Medical Center, Haifa, Israel. 11Department of Respiratory Medicine and Infectious Diseases, Hannover Medical School, Hannover, Germany. 12Biomedical Research in End-Stage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany. 13European Reference Network on Rare and Complex Respiratory Diseases (ERN-LUNG), Frankfurt, Germany. 14Newcastle University and Freeman Hospital, Newcastle, UK. 15Dr Trueta University Hospital, IDIBGI UdG, Girona, Spain. 16Hôpital Cochin, AP-HP and Université Paris Cité, Inserm U1016, Institut Cochin, Paris, France. 17Hospital Clinic of Barcelona, Spain University of Barcelona, CIBERES, IDIBAPS, Barcelona, Spain. 18Division of Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, and Karolinska Severe Asthma Center, Department of Respiratory Medicine and Allergy, Karolinska University Hospital, and Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. 19Heart and Lung Center, Helsinki University Hospital and University of Helsinki, Helsinki, Finland. 20Clinic for Pulmonary Diseases, University Clinical Center of Serbia, and School of Medicine, University of Belgrade, Belgrade, Serbia. 21Hospital Universitario y Politécnico La Fe, Valencia, Spain. 22Pneumology/ Allergology Division, University of Medicine and Pharmacy Nicolae Testemitanu, Medpark International Hospital, Chisinau, Moldova. 23Faculty of Medicine Novi Sad, University of Novi Sad, Novi Sad, Serbia. 24Institute for Pulmonary Diseases, Sremska Kamenica, Serbia. 25Department of Epidemiology, National Tuberculosis and Lung Diseases Research Institute, Warsaw, Poland. 26Pulmonology Department – Unidade Local de Saúde S. João and Faculty of Medicine, University of Porto, Porto, Portugal. 27Hospital Universitari Vall d’Hebron, Barcelona, Spain. 28University Hospital Leuven, Department of Respiratory Diseases and Department of Chronic Diseases, Metabolism and Aging, BREATHE laboratory, KU Leuven, Leuven, Belgium. 29Department of Internal Medicine and Paediatrics, Faculty of Medicine and Health Sciences, Ghent University, and Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium. 30Respiratory Department, Princess Alexandra Hospital, Harlow, UK. 31Health Promotion, Maternal-Child, Internal Medicine and Specialist Excellence “G. D’Alessandro” University of Palermo, Palermo, Italy. 32Northwest Clinics, Alkmaar, Netherlands. 33Respiratory Department, VITAZ hospitals, St Nikolaas, Belgium. 34Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy. 35Respiratory and Cystic Fibrosis Unit, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico Milano, Milan, Italy. Corresponding author: Michal Shteinberg (michalsh@technion.ac.il)Shareable abstract (@ERSpublications)Sinus involvement is common in bronchiectasis and adversely impacts symptoms, but not hospitalisations or mortality. Nasal polyps are independently associated with type 2 inflammation in bronchiectasis. https://bit.ly/4k43bEDCite this article as: Shteinberg M, Haworth CS, Pollock J, et al. The association between chronic rhinosinusitis, bronchiectasis and type 2 inflammation: an EMBARC registry analysis. ERJ Open Res2026; 12: 01397-2025 [DOI: 10.1183/23120541.01397-2025].AbstractIntroduction Chronic rhinosinusitis (CRS) is a common comorbidity in bronchiectasis. Previous studies suggested that bronchiectasis with CRS is associated with elevated type 2 biomarkers, representing anCopyright ©The authors 2026 https://doi.org/10.1183/23120541.01397-2025 ERJ Open Res 2026; 12: 01397-2025ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE M. SHTEINBERG ET AL. ### Page 3 “eosinophilic bronchiectasis” phenotype. However, whether the association with type 2 inflammation exists in rare aetiologies of bronchiectasis such as primary ciliary dyskinesia (PCD) or immune deficiency is unknown. Our aim was to explore the prevalence of CRS with and without nasal polyposis (CRSwNP and CRSnNP), their impact on bronchiectasis outcomes, and their association with type 2 inflammatory biomarkers in patients with bronchiectasis of various aetiologies.Methods Using data from the EMBARC bronchiectasis registry, we classified patients with bronchiectasis as having no CRS, CRSnNP or CRSwNP. Regression models were used to test the effect of CRS on symptom scores and long-term outcomes. Multivariate models were created for elevated “type 2 biomarkers”, defined as elevated blood eosinophil count or total IgE.Results Among 16 640 people with bronchiectasis, 2703 (20.9%) had CRSnNP and 1223 (7.3%) had CRSwNP. CRSwNP and CRSnNP were associated with worse symptoms and more frequent exacerbations, but lower hospitalisations and mortality. Type 2 biomarkers were elevated in people with comorbid CRSwNP in idiopathic bronchiectasis, but not in bronchiectasis secondary to PCD or immune deficiency. In multivariable analysis, CRSwNP was independently associated with elevated type 2 biomarkers.Conclusions CRS and nasal polyposis are common comorbidities in bronchiectasis, associated with worse symptoms and exacerbations. Elevated type 2 biomarkers are associated with CRS, but this finding is dependent on the aetiology of bronchiectasis.IntroductionBronchiectasis is a chronic airway inflammatory condition that is frequently associated with multiple respiratory and nonrespiratory conditions. Chronic rhinosinusitis (CRS), defined by persistent upper airway symptoms and presence of radiological or endoscopic findings of sinus inflammation [1], is reported to affect 32% to 75% of people with bronchiectasis [2–5]. This prevalence is significantly higher than the general population prevalence of CRS estimated as 5–10% [6]. While the association of bronchiectasis with CRS suggests that common pathways may be contributing to both airway diseases, the mechanism of the association between bronchiectasis and CRS is elucidated only for a minority of patients. Examples are a disturbance to mucociliary function in primary ciliary dyskinesia (PCD) [7], CFTR dysfunction in cystic fibrosis (CF) or atopy in asthma with CRS that are responsible for both bronchial and sino-nasal disorders. However, in most cases of bronchiectasis, there is no clear explanation for the association with CRS, although a “united airway” hypothesis with inflammation involving the upper and lower airways has been suggested [2, 8]. Recent research identified an “eosinophilic” subtype of bronchiectasis marked by elevated blood eosinophils in ∼22% of individuals with bronchiectasis [9]. Type 2 inflammation is also a hallmark of CRS, particularly CRS with nasal polyposis (CRSwNP) [6, 10]. It is therefore reasonable that people with bronchiectasis and CRS may be enriched in the eosinophilic bronchiectasis phenotype. In a previous single-centre study we have shown that comorbid CRS among people with bronchiectasis is associated with elevated levels of IgE and blood eosinophils, suggesting a role for “type 2” inflammation in CRS-bronchiectasis [5]. In a subsequent study we have shown that people with CRS and idiopathic or post-infective bronchiectasis have elevated sputum eosinophils. Asthma was excluded by reversibility and methacholine testing, confirming the “eosinophilic bronchiectasis” phenotype as being distinct from asthma [11]. However, the latter study excluded people with aetiologies which may be associated with upper airway involvement by mechanisms other than type 2 inflammation, importantly PCD and immune deficiency, and therefore it is unknown whether type 2 inflammation is a common phenomenon in CRS-bronchiectasis. Identification of clinical phenotypes that are associated with type 2 inflammation is important for tailoring treatments, including monoclonal antibodies, for bronchiectasis that may target inflammation [12, 13]. EMBARC is a multinational prospective registry that recruited and is prospectively collecting information on thousands of people with bronchiectasis in Europe and Israel [14, 15]. EMBARC is to date the largest dataset of patients with bronchiectasis, allowing us to explore endotypes and outcomes of bronchiectasis in a multinational cohort, setting the basis for interventional studies. Given the limitations of single-centre studies in addressing the prevalence, characteristics and impact of comorbid CRS on bronchiectasis, we sought to explore the characteristics and impact of concomitant CRS and nasal polyposis (NP) on patients with bronchiectasis in the EMBARC international, prospective database. Additionally, we sought to test our hypothesis that CRS and NP are associated with type 2 inflammatory biomarkers in people with bronchiectasis.MethodsDetails of the EMBARC bronchiectasis patient registry were previously published [14], and study documents are available at: https://bronchiectasis.hicservices.dundee.ac.uk/registry. Briefly, patients overThis version is distributed under the terms of the Creative Commons Attribution Non- Commercial Licence 4.0. For commercial reproduction rights and permissions contact permissions@ersnet.org Received: 10 Oct 2025 Accepted: 22 Jan 2026https://doi.org/10.1183/23120541.01397-2025 2 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 4 18 years of age with bronchiectasis on chest computed tomography (CT) scan and symptoms compatible with bronchiectasis (cough, sputum production) were recruited after providing signed informed consent, while exclusion criteria were a diagnosis of CF or traction bronchiectasis secondary to idiopathic pulmonary fibrosis. Data collected at baseline include demographic, aetiology and associated comorbidities including CRS and NP, lung function, radiology and sputum microbiology. All centres obtained ethics approval locally.Data collectionPatient enrolment into the EMBARC study began in January 2015 and with recruitment being open-ended and currently ongoing. Patients enrolled up to April 2022 were included for this analysis, with data extracted in June 2024. Patient data were collected annually using a standardised case report form. Daily sputum production was estimated as millilitres per·day, with sputum purulence scored according to MURRAY et al. [16]. Spirometry was performed according to American Thoracic Society/European Respiratory Society standards and predicted values calculated using Global Lung Function Initiative (GLI) equations [17], which were performed at the host site using raw data. The attending physician/medical team recorded bronchiectasis aetiology and verified it using results of aetiological testing [18]. Sputum samples sent during clinical stability and exacerbations were collected, and patients were classified according to specific bacteria isolated from respiratory samples in the previous 12 months. Radiological severity was assessed using the patient’s most recent high-resolution computed tomography scan using the modified Reiff score as previously described [19]. Disease severity was evaluated using the bronchiectasis severity index (BSI) [20] and FACED [21] scores. Exacerbations were defined as use of antibiotics for acute respiratory symptoms and were recorded using patient history, hospital and prescription records [22]. Symptoms were evaluated using the Quality-of-Life Bronchiectasis Questionnaire version 3.1 (with validated translations into native languages) [23].Identification of CRS without nasal polyposis and CRS with nasal polyposisWe identified patients with CRS in the EMBARC registry as being marked positive to the item: (presence of ) “rhinosinusitis” in the EMBARC e-CRF “BRONCHIECTASIS BACKGROUND INFORMATION”page ( per investigator decision), while patients with a negative mark in the same item were regarded as having bronchiectasis without CRS. Similarly, NP was identified in the EMBARC e-CRF. Differences in registry-collected parameters between patients without CRS, and with CRS without (CRSnNP) and with nasal polyposis (CRSwNP) were analysed. Type 2 biomarkers were defined as either elevated blood eosinophils (measured during stability above the locally defined upper limit of normal) or total IgE⩾150 IU·mL−1.Statistical analysisStatistical analysis was performed using IBM statistics (SPSS) v. 24. The continuous variables were presented by mean and standard deviation or median and interquartile range (IQR). The categorical variables were presented in percentages. Demographic and clinical characteristics were compared between patients with and without concomitant CRS and NP. The Chi Square test or Fisher exact test for the categorical variables and one-way ANOVA or Kruskal–Wallis for the continuous variables followed by independent t-test or Mann–Whitney U-test, respectively, for pairwise comparisons with Bonferroni correction were applied consistently. Associations between CRS and the different outcomes were analysed using multivariable analyses performed for the following outcomes: quality of life scores (multiple linear regression), exacerbations and hospitalisations (negative binomial model), and mortality (Cox proportional hazards regression) with CRSnNP and CRSwNP included in the variables and adjustment to various confounders. We assessed elevated type 2 biomarkers –blood eosinophils or total IgE – or one of the former biomarkers by logistic regression with CRSnNP and CRSwNP as well as confounders including aetiologies of bronchiectasis included in the variables. The proportional hazards assumption was checked with inspection of log versus log plots. For the multiple linear regression models, residuals were examined for linearity and homoscedasticity using residual-versus-fitted values plots.ResultsPrevalence of CRSnNP and CRSwNP among people with bronchiectasis of different aetiologiesThe EMBARC registry included 16 640 people with bronchiectasis who had information regarding CRS as of April 2022. Of these, 2703 (20.9%) had CRSnNP and 1223 (7.3%) had CRSwNP (figure 1). Supplementary figure S1 shows the distribution of CRS (either with or without NP) throughout the different countries in the registry, and figure 2 shows the prevalence of CRS, with and without NP, of the different aetiologies of bronchiectasis. The aetiologies most commonly associated with CRS were PCD,https://doi.org/10.1183/23120541.01397-2025 3 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 5 asthma, immunodeficiency and allergic bronchopulmonary aspergillosis (ABPA) with prevalences of CRSnNP and CRSwNP of 33.5% and 30.9% (PCD), 18.4% and 15.6% (asthma), 24.9% and 5.3% (immunodeficiency), and 16.6% and 12.9% (ABPA), respectively.Demographics and impact of CRS and CRSwNP on the severity of bronchiectasisTable 1 shows the baseline demographics for people without CRS, and with CRSnNP and CRSwNP. People with CRS were younger than people without CRS and had fewer comorbidities. As in most bronchiectasis cohorts, bronchiectasis has a female dominance. However, people with CRSnNP had a stronger female dominance, while people with CRSwNP had a weaker female dominance compared to no CRS. Smoking ( past and current) was less prevalent in people with CRS than without CRS. Presence of CRS was associated with increased sputum production and sputum purulence, and more frequent exacerbations. However, compared to no CRS, exacerbations leading to hospitalisations were less common among CRSnNP and intermediate with CRSwNP. Compared to no CRS, patients with CRSnNP and with CRPwNP were more often treated with airways clearance, inhaled corticosteroids (ICS), macrolides and inhaled antibiotics (supplementary table S1). Chronic bacterial infection was more prevalent among people with bronchiectasis and comorbid CRS, while the percentage of individuals without available sputum cultures were similar between the three groups: 25.0% to 27.1% (figure 3). People with bronchiectasis without CRS had the highest proportion of people in the severe disease category in two composite severity scores (BSI and FACED) compared to people with CRSnNP and CRSwNP (figure 4).Impact of CRS on baseline and long-term outcomes of bronchiectasisWe assessed the impact of CRS and NP on several outcomes of bronchiectasis including respiratory symptom scores (assessed by the Quality of Life-B questionnaire), exacerbations at baseline and during follow-up, hospitalisations, and mortality. We composed multivariable analyses for these outcomes, including CRS with and without NP and additional confounders which are known to affect long-term outcomes in bronchiectasis. Compared to no CRS, CRSnNP and CRSwNP were associated with reduced (worse) symptom scores. CRSnNP and CRSwNP were also associated with more frequent exacerbations, but this association did not remain after adjusting to confounders, including those associated with worse severity (such as Pseudomonas bronchial infection and dyspnoea score). CRS with and without NP were associated with less hospitalisations and reduced mortality compared to no CRS (table 2).16 640 individuals with bronchiectasis Stratified by CRS status No CRS: 12 714 BEC tested: 3734 Total IgE tested: 3584 Total IgE tested: 1146 Total IgE tested: 469 BEC tested: 1147 BEC tested: 466 CRSnNP: 2703 CRSwNP: 1223FIGURE 1 Patients included in the analysis according to CRS status with availability of blood eosinophil count (BEC) and total IgE. CRS: chronic rhinosinusitis; CRSnNP: chronic rhinosinusitis without nasal polyps; CRSwNP: chronic rhinosinusitis with nasal polyps. https://doi.org/10.1183/23120541.01397-2025 4 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 6 Association of CRS with markers of type 2 inflammation in bronchiectasisWe next examined the association of type 2 biomarkers (elevated blood eosinophil count (BEC) and total IgE) with CRS. 7922 individuals had information on BEC, and 7594 had data on total IgE levels. 6859 patients had data on both T2 biomarkers. Among people with idiopathic and post-infectious bronchiectasis (which constitute the majority of adults with bronchiectasis), CRSnNP and CRSwNP were significantly associated with increased prevalence of elevated BEC. However, BEC and IgE levels were not differentially distributed among CRS groups among patients with bronchiectasis secondary to PCD or immune deficiency. CRS was associated with elevated levels of total IgE only among people with idiopathic bronchiectasis. People with idiopathic and post-infective bronchiectasis with comorbid CRS were more frequently tested for ABPA compared to no CRS, but there was no difference in the per cent of people fulfilling criteria for ABPA. In people with idiopathic bronchiectasis, comorbid CRSnNP and CRSwNP were associated with the presence of anti-neutrophil antibodies (ANCA) compared with no CRS (figure 5 and supplementary table S2). We next examined the association of elevated type 2 biomarkers, defined as elevated BEC, total IgE⩾150 IU·mL−1 or either of these biomarkers, with CRS and other comorbidities of bronchiectasis. Factors independently associated with elevated type 2 biomarkers included ABPA, asthma, CRSwNP and COPD. Factors associated with a lower prevalence of elevated type 2 biomarkers were female sex, and aetiologies (compared to idiopathic) of connective tissue disease, PCD and post-infective (figure 6 and supplementary table S2).DiscussionIn this analysis of 16 640 people with bronchiectasis in the EMBARC registry, we confirmed that concomitant CRS, with or without NP, is found with increased prevalence compared to the reported70 60 7.2 16.5 Idiopathic (6423) With comorbidity within aetiologic group (%) Post-infective (3590) COPD (1348) Asthma (1130) Tuberculosis (825) Immunodeficiency (694) Primary ciliary dyskinesia (498) ΑΒΡΑ (459) Rheumatoid arthritis (452) GORD/aspiration (272) Others (210) NTM (168) Inflammatory bowel disease (152) α1-antitrypsin def (107) Obstructive (18) Total (16 640) 15.9 2.7 CRS without nasal polyps % CRS with nasal polyps % 7.7 18.4 2.5 5.3 33.5 12.9 16.6 4.9 3.3 4.3 22.4 2.4 16.7 5.9 22.4 2.8 17.8 11.1 7.3 20.9 5.6 15.1 12.4 24.9 30.9 8.6 15.6 5.8 50 40 30 20 10 0FIGURE 2 Prevalences of comorbid CRS with and without nasal polyps, by aetiology of bronchiectasis. Numbers next to each aetiology represent the total number of individuals with the aetiology in the registry. Numbers in the chart represent percentages with the comorbidity within people with the aetiology. α1-antitrypsin def: α1-antitrypsin deficiency; ABPA: allergic bronchopulmonary aspergillosis; GORD: gastro-oesophageal reflux disease; NTM: nontuberculous mycobacterial infection. https://doi.org/10.1183/23120541.01397-2025 5 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 7 prevalence in the general population without bronchiectasis [1]. However, this prevalence is widely distributed among centres and aetiologies of bronchiectasis. While CRSnNP has a mixed pathogenesis and is more prevalent in women, CRSwNP is associated with elevated type 2 biomarkers and male sex [6]. These characteristics remained similar among people with bronchiectasis with comorbid CRSnNP and CRSwNP, showing significant differences in demographics and elevated type 2 biomarkers. Congestion of the nose and sinuses may lead to “post-nasal drip”, in turn increasing the mucus present and expectorated from the lower airways. It is possible that the observed increased volume and purulence of secretions, as well as increased bacterial infection and exacerbations, may be a consequence of upper airways inflammation, despite more preserved lung function in people with CRS compared to no CRS. An alternative explanation may be higher levels of interleukin (IL)-13 and IL-4 which were found to be associated with type 2 inflammation and affect goblet cell hyperplasia and sputum production [24, 25]. Indeed, we found that comorbid CRS with and without NP are associated with increased respiratory symptoms and exacerbations, but fewer hospitalisations and lower mortality. CRS and NP are associated with increased rates of airway infection. A recent analysis of the EMBARC-BRIDGE cohort showed that upper airways dysbiosis is associated with bronchiectasis severity and that Pseudomonas abundance in the nasopharynx is corelated with its identification in sputum cultures [26], providing a potential mechanism for the observation that bronchiectasis patients with CRS have increased airway bacterial infection. This discrepancy between a higher symptom burden but milder disease severity (reflected by better lung function, lower hospitalisations, higher severity scores and lower mortality rates in people with concomitant CRS) may be explained by a symptom burden increased by concomitant upper airways symptoms, prompting early and frequent treatment (for example, with preventive or acute antibiotics and airway clearance – supplementary table S1) and thus protecting against hospitalisations and mortality. Indeed, airway clearance has been demonstrated to be utilised more often in symptomatic patients with bronchiectasis [27], and similar findings of lower mortality in those treated with ICS were found in people with bronchiectasis and concomitant asthma compared to bronchiectasis with no asthma [28]. Compared to CRSnNP, CRSwNP has greater severity and, hence, an intermediate hospitalisation rate (25.0%, between that of no CRS 28.0% and CRSnNP 20.4%). To note, exacerbations and hospitalisations recorded in EMBARC are those that are attributed to bronchiectasis, not CRS; however, in clinical practice distinguishing between upper and lower airways involvement as a cause of exacerbation may be difficult.TABLE 1 Baseline demographic characteristics and severity scores among patients with and without concomitant CRS and nasal polypsNo CRS CRS without nasal polyps CRS with nasal polyps p-value Patients, n 12 714 2703 1223Age yearsMean±SD 65.2 (14.0) 61.4 (14.9) 58.9 (16.2) <0.001#,¶,+ Median (IQR) 68 (58–75) 65 (54–72) 63 (49–71)Female sex, n (%) 7688 (60.5%) 1773 (65.6%) 666 (54.5%) <0.001#,¶Number of comorbidities, median (IQR) 1 (0–2) 1 (0–2) 0 (0–2) <0.001#,¶,+Number with concomitant asthma, n (%) 3509 (27.6%) 1021 (37.8%) 661 (54.0%) <0.001#,¶,+Number with concomitant COPD, n (%) 3562 (28.0%) 489 (18.1%) 204 (16.7%) <0.001#,¶BMI kg·m−2, median (IQR) 24.9 (21.7–28.7) 24.6 (21.5–28.2) 25.2 (22.4–28.6) 0.012#,+FEV1 % predicted, median (IQR) 75.7 (54.2–95.9) 81.4 (62.2–1.00) 75.6 (58.3–94.6) <0.001#,¶,+mMRC dyspnoea score, median (IQR) 1 (0–2) 1 (0–2) 1 (0–2) <0.001#,¶Usual daily sputum volume mL·day−1, median (IQR) 5 (0–20) 10 (2–20) 10 (2–30) <0.001#,¶Do not produce sputum daily, n (%) 3926 (32.1%) 581 (22.8%) 245 (22.5%) <0.001#,¶Sputum purulence score when stable§, median (IQR) 1 (0–2) 2 (1–2) 2 (1–2) <0.001#,¶Patients with exacerbations leading to hospital admission in previous year, n (%)0 exacerbations 3313 (26.1%) 575 (21.3%) 272 (22.2%) p<0.0001 1 exacerbation 2441 (19.2%) 517 (19.1%) 191 (15.6%) 2 exacerbations 2262 (17.8%) 506 (18.7%) 193 (15.8%)⩾3 exacerbations 4698 (37.0%) 1105 (40.9%) 569 (46.5%)Reiff CT score, median (IQR) 3 (2–6) 3 (2–6) 4 (2–6) <0.001¶,+Ex-smokers, n (%) 5307 (41.7%) 934 (34.6%) 408 (33.4%) <0.001#,¶Current smoking, n (%) 912 (7.2%) 124 (4.6%) 39 (3.2%) <0.001#,¶ CRS: chronic rhinosinusitis; BMI: body mass index; FEV1: forced expiratory volume in 1 s; mMRC: modified Medical Research Council; CT: computed tomography. #: significant difference after Bonferroni correction between no CRS and CRS without nasal polyps; ¶: significant difference after Bonferroni correction between no CRS and CRS with nasal polyps; +: significant difference after Bonferroni correction between CRS without nasal polyps and CRS with nasal polyps; §: sputum purulence score [16]. https://doi.org/10.1183/23120541.01397-2025 6 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 8 Both CRSwNP and CRSnNP were associated with elevated BEC and total IgE levels, an association which remained significant only for CRSwNP when adjusted for multiple confounders. This finding aligns with the well-established understanding that CRSwNP is predominantly a type 2 inflammatory subtype of CRS [29], whereas in CRSnNP, type 2 inflammation is less prominent [30]. In our study, the association with type 2 inflammation may be driven by the largest aetiologic group: these with unknown (idiopathic)60.0 ***,#,¶,+ ***,#,¶,+ ***,#,¶ ***,#,¶ ***,#,¶ *,¶ **,# **,# Airway pathogen isolation No CRS (n=12 714) CRS without nasal polyps (n=2703) CRS with nasal polyps (n=1223) 50.0 40.0 30.0 20.0 10.0 0.0 Any bacterial colonisation Frequency (%)Pseudomonas aeruginosa Hemophilus influenzae Moraxella catarrhalisEnterobacteriaceaeStaphylococcus aureus Streptococcus pneumoniae Stenotrophomonas sp.AspergillusFIGURE 3 Frequency of isolation of bacterial pathogens from respiratory secretions (sputum or bronchoalveolar lavage) according to presence of chronic rhinosinusitis and nasal polyps. CRS: chronic rhinosinusitis. *p<0.05; **p<0.01; ***p<0.001. #: significant difference after Bonferroni correction between no CRS and CRS without nasal polyps; ¶: significant difference after Bonferroni correction between no CRS and CRS with nasal polyps; +: significant difference after Bonferroni correction between CRS without nasal polyps and CRS with nasal polyps.100 % % 36.7% 34.9% 28.2% 9.3% 34.9% 55.6% 5.4% 30.6% 63.8% 5.5% 26.7% 67.5% 29.7% 38.2% 31.9% 32.3% 38.3% 29.1% No CRS (n=12 714) CRS without nasal polyps (n=2703) CRS with nasal polyps (n=1223) No CRS (n=12 714) CRS without nasal polyps (n=2703) CRS with nasal polyps (n=1223) 90 80 70 60 50 40 30 20 10 Mild BSI Moderate BSI Severe BSI Mild FACED Moderate FACED Severe FACED 0 100 90 80 70 60 50 40 30 20 10 0 BSI severity categories# FACED severity categories¶FIGURE 4 Distribution of bronchiectasis severity scores – BSI (bronchiectasis severity index) and FACED (FEV1, Age, Chronic bacterial infection, Extent (radiographic), Dyspnoea) – according to presence of CRS and nasal polyps. #: p<0.001 with significance after Bonferroni corrections between no CRS and CRS with nasal polyps, and between no CRS and CRS without nasal polyps; ¶: p<0.001 with significance after Bonferroni corrections between all comparisons. https://doi.org/10.1183/23120541.01397-2025 7 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 9 TABLE 2 Multivariable models for the association between chronic rhinosinusitis (CRS) and the different outcomesMultivariable model adjusted for BSI and sex Multivariable model – fully adjusted# Parameter No CRS (ref) CRS without nasal polyps CRS with nasal polyps No CRS (ref) CRS without nasal polyps- CRS with nasal polyps- Respiratory symptom score (points) 1.00 −2.85 (−1.79– −3.91) −2.26 (−0.81– −3.70) 1.00 −2.58 (−1.60– −3.56) −2.23 (−0.88– −3.59) Baseline exacerbations (total) 1.00 1.47 (1.33–1.62) 1.77 (1.54–2.04) 1.00 0.98 (0.92–1.05) 1.00 (0.91–1.11)Exacerbations at follow-up (total) 1.00 0.97 (0.91–1.04) 1.04 (0.94–1.14) 1.00 0.96 (0.89–1.03) 1.06 (0.96–1.17)Exacerbations that resulted in hospitalisations 1.00 0.69 (0.62–0.78) 0.70 (0.60–0.82) 1.00 0.69 (0.61–0.78) 0.72 (0.61–0.84) Mortality 1.00 0.80 (0.66–0.96) 0.68 (0.50–0.91) 1.00 0.80 (0.66–0.98) 0.75 (0.56–1.02)Multivariable models of various outcomes with CRS with and without nasal polyps, where no CRS is the reference group. Values are odds ratios or beta coefficients (for respiratory symptom score) with 95% confidence intervals. Bold type indicates that 95% CI values do not contain 1.0. #: adjusted for age, sex, Pseudomonas aeruginosa chronic infection, Medical Research Council dyspnoea score, body mass index, asthma, COPD, smoking, aetiology, region and Reiff score. https://doi.org/10.1183/23120541.01397-2025 8 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 10 bronchiectasis. However, people with PCD have upper and lower airway dysfunction due to a primary defect in mucociliary clearance, with resulting airway neutrophilic inflammation [31, 32]. Other etiologies, such as immune deficiency, were also not found to be associated with type 2 biomarkers, and the mechanism underlying CRS and bronchiectasis may be hypogammaglobulinaemia and an increased tendency for infectious complications [33]. Given the female dominance in asthma, an unexpected finding among people with bronchiectasis is that female sex was negatively associated with elevated type 2 biomarkers. Male sex and eosinophilic bronchiectasis are less common characteristics of bronchiectasis; that these two less common characteristics merge in the same individuals may point to a pathophysiological mechanism yet to be elucidated. However, male sex has been previously described to be associated with eosinophilia in bronchiectasis [9], and several eosinophilic syndromes have male predominance, namely, eosinophilic oesophagitis [34], eosinophilic granulomatosis with polyangiitis [35] and hypereosinophilic syndromes [36]. While BEC has utility in assessing type 2 inflammation in airway diseases, it is an imperfect surrogate of airway eosinophil counts as has been demonstrated in bronchiectasis [9], asthma [37] and COPD [38]. Although not supported by randomised controlled trials, several reports suggest the efficacy of type 2 directed treatments including ICS and biologic treatments in people with “eosinophilic bronchiectasis” [12, 13]. Due to the limitations of the BEC as a biomarker of type 2 inflammation, it is therefore important that clinicians recognise clinical factors associated with elevated type 2 inflammation in bronchiectasis, including CRS. Our findings suggest that we should actively investigate the presence of type 2Total IgE: idiopathic BE# NS 25 a) c) d) e) b) 10.3% 84.7% 11.7% 82.7% 14.6% 7.7% 5.9% 4.5% 9.6% 11.1% 80.6% 5.5% 87.8%95.5% 79.8%79.2% 87.9% 87.4% 20 15 10 5 0 PCD n=1121 NoCRS n=300 CRSnNP n=96 CRSwNP n=248 NoCRS n=119 CRSnNP n=22 CRSwNP n=94 NoCRS n=108 CRSnNP n=98 CRSwNP No CRS (%) CRS without nasal polyps (%) CRS with nasal polyps (%) Immune deficiency Idiopathic Post-infectious n=2121 No CRS <150 >2000 IgE levels IU·mL−1 150–500 501–1000 1001–2000 3.1% 12.0% 81.7% 4.7% 13.2% 79.2% 5.5% 19.8% 70.4% n=619 CRSnNP n=253 CRSwNP With elevated BEC (%)With IgE range (%) With IgE range (%) With IgE range (%) With IgE range (%) p=0.06 p<0.001 Elevated blood eosinophils (BE) Total IgE: post-infectious BE¶ Total IgE: Immune deficiency¶ Total IgE: PCD¶ p<0.001FIGURE 5 a) Percentage of individuals with elevated blood eosinophil counts according to presence of chronic rhinosinusitis and nasal polyps and different aetiologies of bronchiectasis. b–e) Total IgE level distribution according to the presence of chronic rhinosinusitis and nasal polyps and different aetiologies of bronchiectasis. Numbers under each bar represent total number of individuals with total IgE measurements. PCD: primary ciliary dyskinesia; BEC: blood eosinophil count; CRS: chronic rhinosinusitis; CRSnNP: chronic rhinosinusitis without nasal polyps; CRSwNP: chronic rhinosinusitis with nasal polyps. #: p<0.001; ¶: nonsignificant. https://doi.org/10.1183/23120541.01397-2025 9 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 11 Age Eosinophils only IgE only Eosinophils or IgE 1.00 (0.99–1.00) 1.00 (0.99–1.00) 0.51 (0.45–0.58) 1.01 (0.89–1.15) 1.50 (1.16–1.94) 0.80 (0.67–0.94) 0.80 (0.57–1.11) 0.56 (0.29–1.06) 16.60 (12.40–22.10) 0.96 (0.65–1.42) 0.72 (0.52–0.99) 2.24 (1.93–2.83) 1.21 (0.94–1.56) 0.64 (0.37–1.11) 0.75 (0.35–1.61) 0.41 (0.18–1.96) 0.69 (0.37–1.29) 1.10 (0.95–1.28) 1.21 (1.00–1.49) 1.00 (0.99–1.01) 0.55 (0.49–0.62) 1.04 (0.93–1.18) 1.28 (0.99–1.65) 0.86 (0.74–1.00) 0.77 (0.57–1.03) 0.64 (0.48–1.09) 19.90 (13.90–28.60) 1.01 (0.72–1.43) 0.62 (0.46–0.84) 2.42 (2.00–2.93) 1.23 (0.97–1.57) 0.70 (0.44–1.12) 0.66 (0.33–1.31) 0.45 (0.23–0.88) 0.79 (0.47–1.34) 1.04 (0.91–1.19) 1.57 (1.30–1.90) 0.67 (0.58–0.78) 1.03 (0.88–1.20) 0.92 (0.66–1.29) 0.98 (0.80–1.19) 0.72 (0.47–1.12) 0.70 (0.32–1.53) 7.52 (5.92–9.55) 1.08 (0.69–1.70) 0.55 (0.35–0.86) 2.39 (1.91–3.00) 1.08 (0.78–1.51) 0.63 (0.30–1.30) 0.62 (0.22–1.73) 0.57 (0.23–1.43) 0.88 (0.42–1.85) 1.11 (0.93–1.33) 2.06 (1.66–2.55) Odds ratio (log scale) Odds ratio (log scale)Odds ratio (log scale) Female sex Ex-smoker Current smoker Post-infective TB NTM ABPA Rheumatoid arthritis PCD Asthma COPD GORD/aspiration A1AT deficiency Connective tissue disease IBD CRSnNP CRSwNP Age Female sex Ex-smoker Current smoker Post-infective TB NTM ABPA Rheumatoid arthritis PCD Asthma COPD GORD/aspiration A1AT deficiency Connective tissue disease IBD CRSnNP CRSwNP Age Female sex Ex-smoker Current smoker Post-infective TB NTM ABPA Rheumatoid arthritis PCD Asthma COPD GORD/aspiration A1AT deficiency Connective tissue disease IBD CRSnNP CRSwNP 100 101 100 101 100 101FIGURE 6 Odds ratio for elevated type 2 biomarkers: logistic regression with dependent variables: elevated blood eosinophils; elevated total IgE ⩾150 IU·mL−1; either elevated blood eosinophils OR total IgE ⩾150 IU·mL−1. X-axis is plotted on a logarithmic scale. Current and ex-smokers are compared to never-smokers. Aetiologies – post-infective, tuberculosis (TB), NTM, ABPA, rheumatoid arthritis, PCD, asthma, COPD, GORD/aspiration, A1AT deficiency, connective tissue disease and IBD – are compared to idiopathic (reference). CRSnNP and CRSwNP are compared to no CRS (reference). ABPA: allergic bronchopulmonary aspergillosis; CRS: chronic rhinosinusitis; PCD: primary ciliary dyskinesia; CRSnNP: chronic rhinosinusitis without nasal polyps; CRSwNP: chronic rhinosinusitis with nasal polyps; GORD: gastro-oesophageal reflux disease; IBD: inflammatory bowel disease; NTM: nontuberculous mycobacterial infection. https://doi.org/10.1183/23120541.01397-2025 10 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 12 inflammation in these selected subtypes of bronchiectasis demonstrated to be enriched in type 2 inflammation, even when BEC are not overtly elevated. Previous work reported that CRS precedes bronchiectasis by 6 years or more and suggested that CRS may cause bronchiectasis [39, 40]. However, regardless of proof of causation, given the association of CRS with bronchiectasis described by this and previous studies, we suggest that lower respiratory symptoms (cough, sputum production, lower respiratory tract infections) should prompt an investigation of bronchiectasis by referral to high-resolution chest CT in people with CRS. We acknowledge several limitations that result from the methodology of our study. Importantly, the presence of CRS and NP were extracted from the EMBARC registry entry questionnaire as determined by the EMBARC investigators and not validated according to established criteria [1]. Investigators may have different interests in upper airway symptoms which may reflect differential recordings of the diagnoses. Second, BEC and total IgE were not uniformly available, and we did not have access to additional type 2 biomarkers including sputum eosinophil counts, specific IgE levels, fractional excreted NO or skin testing for inhaled allergens. Further, immune deficiency may have multiple causes, primary and secondary, which may have different mechanisms by which bronchiectasis develops. In this analysis we grouped immunodeficiencies together due to the relatively small number of patients with immunodeficiencies in the registry. Major strengths of our work were a large, international and prospective registry with long-term follow-up that has a representation of rare aetiologies, enabling us to investigate the impact and the characteristics of comorbid CRS and NP by aetiology. In conclusion, we demonstrate that CRS and NP are a common comorbidity in bronchiectasis; their presence carries adverse consequences on quality of life, chronic airway infection and exacerbations in bronchiectasis, and are associated with elevated type 2 biomarkers. This may be a useful biomarker in future studies of type 2 directed treatments (including biologic treatment) in bronchiectasis. That CRS and NP are an aetiology of “eosinophilic bronchiectasis” may be hypothesised and remains to be investigated.Provenance: Submitted article, peer reviewed. During the preparation of this work the authors used ChatGPT 4.0 in order to generate figure 6. After using this tool, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication. Author contributions: Study conception and design: M. Shteinberg and J.D. Chalmers; data collection: A. Shoemark, K. Robertson, A. De Soyza, F.C. Ringshausen, P.C. Goeminne, N. Lorent, C.S. Haworth, M.R. Loebinger, M. Shteinberg, S. Aliberti, E. Polverino, O. Sibila, and J.D. Chalmers; data analysis: N. Stein, M. Shteinberg, A. Shoemark and J.D. Chalmers; writing of the manuscript: M. Shteinberg and J.D. Chalmers; revising critically for important intellectual content and final approval: all authors Conflict of interest: M. Shteinberg reports grants or contract from the Tel Aviv League for Lung Disease and the G. Baum Foundation, paid to her institution; personal payments for consultation from AstraZeneca, Boehringer Ingelheim, Dexcel, Kamada, Synchrony Medical, Trumed and Zambon; personal payments or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from AstraZeneca, Boehringer Ingelheim, GSK, Kamada, Sanofi and Insmed; support for attending meetings and/or travel from Boehringer Ingelheim Israel, Astra Zeneca Israel, Kamada, Rafa and GSK Israel; personal fees for participation on a data safety monitoring or advisory board from Bonus Biotherapeutics, Boehringer Ingelheim, AstraZeneca and Insmed; personal payments as an American Journal of Respiratory and Critical Care Medicine associate editor; and voluntary roles as a Journal of Cystic Fibrosis associate editor, a management board member of the Israeli Pulmonology Society and the Israeli society for Tuberculosis and Mycobacterial Diseases, a management board member of EMBARC, an editorial board member of the European Respiratory Journal, and a member of the European Respiratory Society task forces on bronchiectasis guidelines and transitioning in bronchiectasis, all in the past 36 months. C.S. Haworth reports grants or contracts from AstraZeneca to his institution; personal fees for consulting from 30 Technology, AstraZeneca, BiomX, Chiesi, Infex, Insmed, LifeArc, Pneumagen, Vertex and Zambon; personal payments or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Chiesi, Insmed, LifeArc, Vertex and Zambon; personal payment for expert testimony from Zambon; is a board member of the European Cystic Fibrosis Society; and owns stock or stock options in Pneumagen, all in the past 36 months. J. Pollock is a member of the early career mentoring programme of this journal. S. Cohen, J. Jrbashyan, N. Abo Helo, N. Stein, Y. Adir, M. Vendrell, H. Lind, K. Viligorska, K. Robertson, P. Kauppi, B. Milenkovic, R. Menendez, O. Munteanu, A. Torres, E. Van Braeckel, M. Anwar and W. Boersma have https://doi.org/10.1183/23120541.01397-2025 11 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 13 nothing to disclose. M.R. Loebinger reports consulting fees from Armata, 30T, AstraZeneca, Parion, Insmed, Chiesi, Zambon, Electromed, Recode, Boehringer Ingelheim, Ethris, Mannkind and AN2 Therapeutics; and payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Insmed, all in the past 36 months. K. Dimakou reports payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Novartis, Boehringer Ingelheim, GSK, NORMA Hellas, Chiesi, AstraZeneca and Zambon; direct payment in support for attending meetings and/or travel from Novartis, Boehringer Ingelheim, GSK, NORMA Hellas, Chiesi, AstraZeneca and Menarini; and direct payment for participation on a data safety monitoring or advisory board from Novartis, GSK and Chiesi, all in the past 36 months. S. Aliberti reports grants or contracts from GSK to his institution; personal fees for consulting from INSMED Incorporated, INSMED Italy, INSMED Ireland Ltd, INSMED Netherlands BV, ZAMBON Spa, AstraZeneca, Menarini, CSL Behring GmbH, Pfizer, Fondazione Internazionale Menarini, Moderna Italy, Moderna TX, Boehringer Ingelheim, Chiesi Farmaceutica Spa, MSD Italia S.r.l., Vertex Pharmaceuticals, BRAHMS GMBH, Physioassist SAS, AN2 Therapeutics, GlaxoSmithKline Spa and Verona; personal payments or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from GlaxoSmithKline Spa, Fondazione Internazionale Menarini, INSMED Italy, INSMED Ireland Ltd, Boehringer Ingelheim, Zambon and Vertex Pharmaceuticals; and personal payments for data safety monitoring or advisory boards from INSMED Incorporated, INSMED Italy, AstraZeneca UK Limited, MSD Italia S.r.l. and Verona pharma plc, all in the past 36 months. F.C. Ringshausen reports grants or contracts from the German Center for Lung Research (DZL), German Center for Infection Research (DZIF), IMI (EUEFPIA) and iABC Consortium (including Alaxia, Basilea, Novartis and Polyphor), Mukoviszidose Institute, Novartis and Insmed Germany to his institution; personal fees for consulting from Parion Sciences, Boehringer Ingelheim, Insmed and Chiesi; personal payments or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from I!DE Werbeagentur GmbH, Insmed, Grifols, University Hospital Hamburg, AstraZeneca, Cliniqo GmbH and Sanofi; personal fees for participation on a data safety monitoring or advisory board from Insmed, Boehringer Ingelheim, Parion Sciences and Chiesi; honorary positions as co-chair of the German Bronchiectasis Registry PROGNOSIS, a member of the SteerCo of the European Bronchiectasis Registry EMBARC and a principal investigator of the DZL; fees for clinical trial participation paid to his institution by AstraZeneca, Boehringer Ingelheim, Insmed, Novartis, Parion Sciences, ReCode, Ruhr University-Bochum, University of Dundee, UMC Utrecht and Vertex, all in the past 36 months. A. De Soyza reports grants or contracts from GSK, 30T and Sanofi to his institution; personal fees for consulting from 30T, Insmed, AstraZeneca and Sanofi; personal payments or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from AstraZeneca, Bayer, GSK, Insmed, Zambon, Sanofi, Fisher & Paykel and Inogen, all in the past 36 months. P.R. Burgel reports personal fees for consulting from AstraZeneca, Boehringer Ingelheim, Chiesi, GSK, Insmed, MSD, Pfizer, Vertex and Viatris; and support for attending meetings and/or travel from AstraZeneca and Chiesi to his institution, in the past 36 months. O. Sibila reports consulting fees from Insmed and Boehringer Ingelheim in the past 36 months. A. Bossios reports that a grant from AstraZeneca was paid his my institution outside the submitted work; honoraria and lecture fees from Chiesi, GSK, and AstraZeneca paid to his institution outside the submitted work; and is Head of Assembly 5 (Airway diseases, asthma, COPD and chronic cough) of the European Respiratory Society (ERS), co-chair of the Nordic Severe Asthma Network, member of the steering committee of SHARP (ERS severe asthma Clinical Research Collaboration) and a member of the steering committee of the Swedish National Airway Register, all in the past 36 months. D. Obradovic reports support for attending the ERS Congress in 2024 and is President of the Serbian Society of Intensive Care Medicine. A. Nowinski reports scientific grants received from the National Centre for Research and Development, the Medical Research Agency and the pharmaceutical industry (Boehringer Ingelheim, GSK and AstraZeneca) to their institutions in the past 36 months. A. Amorim reports grants or contracts from the European Cystic Fibrosis Society Patient Registry; and personal consulting fees and payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Vertex Pharmaceuticals Inc.; support for attending meetings and/or travel from Zambon and Boehringer Ingelheim; and personal fees for participation on a data safety monitoring or advisory board from Chiesi, all in the past 36 months. N. Lorent is a member of the EMBARC management committee. S. Battalglia reports personal fees for advisory boards from GSK and Insmed; personal payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Insmed; and personal support for attending meetings and/or travel from Lusofarmaco and Sapio, all in the past 36 months. A. Shoemark reports that EMBARC3 is supported by Armata, AstraZeneca, Boehringer Ingelheim, Chiesi, CSL Behring, GlaxoSmithKline, Grifols, Insmed, LifeArc, Roche, Verona and Zambon; grants or contracts from AstraZeneca and LifeArc; consulting fees from Spirovant, Translate Bio and ReCode Therapeutics; payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Translate Bio, Ethris and Insmed; unpaid involvement in European Respiratory Society Clinical Research Collaborations (EMBARC, BEATPCD and AMR Lung); and is supported by the Asthma and Lung UK Chair of Respiratory Research, all in the past 36 months. P.C. Goeminne reports payment or honoraria for lectures from Insmed, RMEI, AstraZeneca and GSK; support to attend conferences from GSK and AstraZeneca; participation on a data monitoring committee for Boehringer, and advisory boards for MSD and Pfizer, all in the past 36 months. F. Blasi reports grants from AstraZeneca, Chiesi and Insmed; personal fees for consulting from Menarini; and personal fees https://doi.org/10.1183/23120541.01397-2025 12 ERJ OPEN RESEARCH ORIGINAL RESEARCH ARTICLE | M. SHTEINBERG ET AL. ### Page 14 for lectures and advisory board from AstraZeneca, Chiesi, Boehringer Ingelheim, GSK, Guidotti, Grifols, Insmed, Menarini, Novartis, OM Pharma, Pfizer, Sanofi, Vertex and Zambon, in the past 36 months. E. Polverino reports consulting fees from Insmed, Grifols, Pari and CSL Behring; and payment or honoraria for lectures, presentations, speakers’ bureaus, manuscript writing or educational events from Insmed, Pari, Grifols and CSL Behring, in the past 36 months. J.D. Chalmers reports grants or contracts from AstraZeneca, Genentech, Boehringer Ingelheim, Gilead, Chiesi, Grifols, Insmed and Trudell; and consulting fees from Janssen, Antabio, Pfizer, Zambon, AstraZeneca, Chiesi, GlaxoSmithKline, Insmed, Grifols, Novartis and Boehringer Ingelheim, in the past 36 months and is the Chief Editor of ERJ Open Research. Support statement: This research was funded by the European Respiratory Society through the EMBARC3 Consortium. EMBARC3 is supported by project partners Armata, AstraZeneca, Boehringer Ingelheim, Chiesi, CSL Behring, GlaxoSmithKline, Grifols, Insmed, Lifearc, Roche, Verona and Zambon. Funding information for this article has been deposited with the Open Funder Registry.References 1 Fokkens WJ, Lund VJ, Hopkins C, et al. European position paper on rhinosinusitis and nasal polyps 2020.Rhinology 2020; 58: Suppl. S29, 1–464.2 Guilemany JM, Angrill J, Alobid I, et al. 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