Andreas M. Matthaiou

Background: Wildfires release large amounts of particulate matter and other ambient air pollutants. Acute exposure can exacerbate asthma, chronic obstructive pulmonary disease, and other chronic respiratory diseases. Populations living at the urban–wildland interface are particularly vulnerable. Action: In September 2022, a non-profit initiative supported by the European Lung Foundation Healthy Lungs for Life campaign was organised in wildfire-affected areas of Attica, Greece, aiming to raise awareness of respiratory risks, identify vulnerable individuals, and promote preventive behaviours. Implementation: Outreach stations were set up in community locations affected by extensive summer wildfires. Residents underwent brief structured interviews assessing respiratory symptoms, smoking history, and exposure risk, followed by on-site spirometry to detect previously unrecognised airflow limitation. Personalised counselling on risk reduction, early symptom recognition, and when to seek medical care was provided. Outcomes: Volunteers engaged with more than 100 residents, most aged >50 years. Over half were current or former smokers with significant smoking history and/or daily dyspnoea or chronic cough, indicating a high risk for exacerbations. Individuals with abnormal spirometric indices were advised to seek pulmonology evaluation. Participants reported increased awareness of air quality risks and preventive strategies. Conclusions: This community-based Healthy Lungs for Life action combined education with spirometric screening to identify vulnerable individuals and enhance health literacy in wildfire-prone areas. Similar outreach initiatives may strengthen early detection and community resilience to climate-related respiratory threats.

Background: Exposomic studies in idiopathic pulmonary fibrosis (IPF) have multifacetedly shown that ambient air pollution is associated with both heightened susceptibility to disease development and increased risk of adverse outcomes. Aim and Objectives: We aimed to systematically review the literature about the multidimensional effects of air pollution on IPF, focusing on incidence, chronic symptoms, disease severity and progression, acute and chronic complications, and mortality or lung transplantation. Methods: A systematic review protocol was designed and registered in PROSPERO according to the PRISMA guidelines. The databases MEDLINE via PubMed, Embase, and Scopus were searched up to 2025 for studies investigating the clinical effects of exposure to O₃, CO, NO₂/NO_x, SO₂, PM_0.1 (UFP), PM_2.5, and PM₁₀ in IPF. A qualitative synthesis of the findings followed. Results: A total of 29 studies from 12 different countries (2014–2025) globally (Figure 1A) were included in the review. The most frequently investigated air pollutants and clinical outcomes were NO₂/PM_2.5 and mortality, respectively, while the least frequently were UFP and chronic symptoms, respectively (Figure 1B–C). All air pollutants were variably associated with worse clinical outcomes, except for UFP (*) in only one study (Figure 1D). Conclusions: Air pollution is a multimodal mediator in the natural history of IPF, with adverse effects on the prognosis of the disease, indicating an urgent need for exposure-reduction approaches in these patients. erj;68/suppl_70/PA1679/F1 F1 F1

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive debilitating lung disease which affects physical and mental well-being. The IPF Patient-Reported Outcome Measure (IPF-PROM) scale is a validated and reliable tool for the self-report of physical and psychological well-being in IPF. Aims and objectives: This study aimed to validate a Greek version of the IPF-PROM scale and further investigate its correlation with clinical features of IPF patients and its interrelation with depressive symptoms and health-related quality of life (HRQoL). Methods: This was a two-centre, observational, cross-sectional study, in which IPF patients completed three scales: IPF-PROM, Patient Health Questionnaire-9 (PHQ-9), an index of depressive symptoms, and Health Survey Questionnaire Short Form-12 (SF-12), an index of HRQoL, at the IPF Outpatient Clinics of two University Hospitals in Greece during 2023–2024. Logistic regression analysis was conducted to assess severe status of IPF-PROM compared with mild/moderate status. Results: The study involved 136 IPF patients (87.9% males) with a mean age of 73.5±7.9 years. Patients were classified overall with moderate disease according to IPF-PROM mean scores (41.7±31.3), particularly in the combined Breathlessness/Fatigue and the Psychological well-being components (40.1 and 43.8, respectively, p>0.050). Patients with severe symptoms, as measured by IPF-PROM, scored higher levels of depressive symptoms on PHQ-9 compared with those with moderate or mild symptoms (17.1, 12.3 and 1.4, respectively, p<0.001) and lower levels of HRQoL in physical (32.6, 34.7 and 47.9, p<0.001) and mental health on SF-12 (23.9, 34.5 and 50.3, p<0.001). Patients with incrementally higher levels of oxygen saturation had lower odds for severe health status according to IPF-PROM (OR=0.83, p=0.018). Conclusions: A significant percentage of IPF patients present with impaired health status and symptoms suggestive of depression. The IPF-PROM scale represents a useful tool that may predict impairment of mental health and HRQoL in IPF, with potential utility for clinical practice and research.

Background and Aims: Plasma fibrinogen and fractional exhaled nitric oxide (FeNO) reflect neutrophilic and eosinophilic airway inflammation, respectively, and are associated with disease activity and severity in different directions in bronchiectasis. This study aimed to concurrently investigate fibrinogen and FeNO and further evaluate the clinical importance of fibrinogen-to-FeNO ratio (FFR) as a composite biomarker in bronchiectasis. Methods: This was a two-centre, observational, cross-sectional study involving stable bronchiectasis patients. Fibrinogen, FeNO, and the ratio of their normalised values (FFR) were investigated in relation to clinical indicators of disease activity and severity, including respiratory symptoms, inflammatory markers, pulmonary function, radiological extent, airway infection, severity scores, and patient-reported outcomes. Results: FFR was correlated with both circulating neutrophils (r = 0.36, p = 0.04) and eosinophils (r = −0.39, p = 0.03) and, more strongly compared to fibrinogen and FeNO, with the percentage of predicted forced expiratory volume in the 1st second (r = −0.61, p < 0.001). Interestingly, only FFR was found to be higher in patients with Pseudomonas aeruginosa isolation in respiratory secretions (p < 0.01). In receiver operating characteristic curves, FFR showed good discriminatory ability to differentiate patients with any level (AUC: 0.80, 95% CI: 0.64–0.96) or a severe level (AUC: 0.83, 95% CI: 0.64–1.00) of pulmonary functional impairment and patients with severe disease (AUC: 0.78, 95% CI: 0.62–0.94). Conclusions: FFR emerges as a candidate biomarker capturing the balance between neutrophilic and eosinophilic inflammation and the net disease activity and severity in bronchiectasis.

Pulmonary actinomycosis and pulmonary nocardiosis are rare chronic respiratory infections that may closely resemble lung cancer due to their overlapping clinical, radiological, and bronchoscopic characteristics. This hybrid case series and narrative review aims to elucidate the presenting patterns, diagnostic pathways, management strategies, and practical implications of these infections in the differential diagnosis of lung cancer. We analyzed four consecutive cases managed at the Sotiria Thoracic Diseases General Hospital in Athens from 2021 to 2025, supplemented by eight additional cases identified through a review of Greek grey literature from the same period. In the 12 cases reviewed, patients commonly presented with cough, dyspnea, fever, hemoptysis, malaise, and weight loss. Chest imaging frequently revealed consolidation, cavitation, atelectasis, nodules, or mediastinal lymphadenopathy, often prompting an oncological evaluation. Bronchoscopic findings occasionally mimicked malignant submucosal spread, and increased fluorodeoxyglucose uptake added to the diagnostic uncertainty. Notably, one case exhibited coexistence of pulmonary actinomycosis with lung adenocarcinoma. Microbiological and histopathological evaluations confirmed the diagnoses, and most patients showed clinical and radiological improvement following prolonged targeted antimicrobial therapy. Given these findings, pulmonary actinomycosis and nocardiosis should be considered in patients with suspected lung cancer, particularly when infectious features coexist with mass-like or cavitary lesions. Careful tissue sampling, specialized microbiological testing, and structured follow-up are essential for excluding occult or coexisting malignancy.

Background: Plasma fibrinogen and fractional exhaled nitric oxide (FeNO), as inverse biomarkers, are associated with neutrophilic and eosinophilic inflammation, respectively, in bronchiectasis. We aimed to investigate the clinical importance of fibrinogen-to-FeNO ratio (FFR) in this disease. Methods: In this cross-sectional study, FFR was investigated in 48 stable bronchiectasis patients in relation to clinical indicators of disease activity and severity: inflammatory markers, lung function, radiological extent, airway infection, and severity scores. Results: FFR was more strongly correlated, compared to fibrinogen and FeNO separately, with FEV₁%Pred (r = −0.61, p < 0.001), serum C-reactive protein (r = 0.59, p < 0.001), and circulating neutrophils (r = 0.36, p = 0.04) and eosinophils (r = −0.39, p = 0.03, Fig. 1A–B). It was higher in patients with airway infection by Pseudomonas aeruginosa (p < 0.01, Fig. 1C). In receiver operating characteristic curves (Fig. 1D), FFR showed good discriminative ability to distinguish patients with any level (AUC: 0.80, 95% CI: 0.64–0.96) or severe level (AUC: 0.83, 95% CI: 0.64–1.00) of lung functional impairment or with severe disease (AUC: 0.78, 95% CI: 0.62–0.94). Conclusions: FFR reflects the balance between neutrophilic and eosinophilic inflammation and the net disease activity and severity in bronchiectasis (Fig. 1E). *AMM & NB contributed equally. erjor;12/suppl_18/PS107/F1 F1 F1

This article summarises clinical and research insights into the prevention and therapy of respiratory infections, along with consensus statements and key guideline recommendations reported at the 2025 #ERSCongress https://bit.ly/4qd6BXW

Birt–Hogg–Dubé (BHD) syndrome is a rare genetic disease, inherited in an autosomal dominant manner, that was first described in the mid-1970s and occurs due to pathogenic variants in the folliculin gene (FLCN) on chromosome 17p11.2. The syndrome has numerous clinical manifestations and primarily affects the lungs, kidneys, and skin. As far as the pulmonary features are concerned, more than 80% of patients appear to develop bilateral pulmonary cysts located in the lower lung zones, in the subpleural area, with cumulative risk of spontaneous pneumothorax depending on the number of cysts in the lungs. Another serious feature of the syndrome is the increased risk of renal cell carcinoma, which is often an incidental finding on screening or medical imaging. Cutaneous manifestations include benign fibrofolliculomas, trichodiscomas, and acrochordons (skin tags), which primarily affect the patients’ emotional status as a result of their cosmetic defects. BHD syndrome is generally an underdiagnosed condition due to the great variability of its clinical picture, thus highlighting the importance of genetic testing for FLCN mutations in suspected cases. The application of ERN GENTURIS guidelines in clinical practice can facilitate early, accurate diagnosis of the disease and optimal personalized management of the patients.

Bronchiectasis is a heterogeneous chronic airway disease traditionally viewed as neutrophil-driven. Emerging evidence demonstrates distinct complex inflammatory phenotypes influencing clinical outcomes, prognosis and therapeutic options. A narrative review was conducted, informed by a structured literature search on PubMed and Google Scholar databases, focusing on inflammatory phenotypes in bronchiectasis. Based on the prevalent cellular population, four distinct phenotypes can be described. The most common is the neutrophilic phenotype, which is associated with frequent Pseudomonas infection, severe disease, exacerbations and poor prognosis. Targeted novel-agents for this group such as brensocatib (neutrophil protease inhibition) emerge. The eosinophilic phenotype is defined by elevated blood or sputum eosinophils and is associated with FeNO, IL-5/IL-13 signaling, a possible response to inhaled corticosteroids and biologic agents. The mixed phenotype demonstrates dual neutrophilic and Th2 inflammation. Paucigranulocytic phenotypes remain poorly characterized but with distinct characteristics. Finally, dysregulation of macrophages and lymphocytes as inflammation mediators needs to be studied further. Recent advances have introduced a variety of therapeutic strategies targeting specific inflammatory pathways. Bronchiectasis has a spectrum of inflammatory phenotypes with distinct biological and clinical implications. Recognition and better understanding of inflammatory phenotypes in bronchiectasis may enable opportunities for personalized precision medicine through the transition from empirical management to biomarker-guided, personalized care.