Sean W Harshman, Kiersten J Weatherbie, Alena R Veigl, Anne E Jung, Madison A Stoner-Dixon, Aubrianne I Dash, Christopher J Land, Dylan T Slizewski, Eli F Kelley, Jennifer Schwanekamp-Kerr, Timothy Halverson, Christina N Davidson, Christopher W Myers, Kara J Blacker, Jennifer A Martin, Rhonda L Pitsch
{"title":"Estimating hypoxia-induced brain dysfunction and cognitive decline through exhaled breath monitoring.","authors":"Sean W Harshman, Kiersten J Weatherbie, Alena R Veigl, Anne E Jung, Madison A Stoner-Dixon, Aubrianne I Dash, Christopher J Land, Dylan T Slizewski, Eli F Kelley, Jennifer Schwanekamp-Kerr, Timothy Halverson, Christina N Davidson, Christopher W Myers, Kara J Blacker, Jennifer A Martin, Rhonda L Pitsch","doi":"10.1186/s12931-025-03296-5","DOIUrl":"10.1186/s12931-025-03296-5","url":null,"abstract":"<p><strong>Background: </strong>Hypoxia remains a concern for aircrew operating high performance aircraft. Sensing and mitigating hypoxia is a line of active research within the US Air Force and US Navy. It is hypothesized that changes in exhaled breath volatile organic compound content could indicate, not only changes in oxygen saturation (SpO<sub>2</sub>), but also brain activity and cognitive function.</p><p><strong>Methods: </strong>On-line exhaled breath monitoring via proton transfer reaction mass spectrometry was used to observe changes in volatile organic compound concentrations during mask-free hypoxic exposures. Additionally, electroencephalography measurements in response to an odd-ball paradigm and cognitive tasks were collected throughout the exposures.</p><p><strong>Results: </strong>The data show hypoxic exposures induced a physiological response including a significant reduction in SpO<sub>2</sub>, a decrease in the electroencephalography waveform peak-to-peak amplitude (p < 0.05), a significant increase in psychomotor vigilance test response time, and an increase in perceived symptomatology. Exhaled breath results indicate 19 volatile organic compound features are significantly different between hypoxia and normoxia (p < 0.05) with 13 showing an increase in exhaled breath compared to background measurements (p < 0.05). Linear mixed modeling with stepwise reduction demonstrates 7 of the features are significantly indicative of changes in SpO<sub>2</sub> with 3 and 4 features indicative of changes in brain wave functions and psychomotor vigilance test response times, respectively.</p><p><strong>Conclusions: </strong>The data establish, for the first time, differences in exhaled breath volatile concentrations that indicate changes in cognition derived from hypoxic insult.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"215"},"PeriodicalIF":5.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144295188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Liyuan Dai, Liling Huang, Lin Li, Le Tang, Yuankai Shi, Xiaohong Han
{"title":"Unraveling the role of HDAC3 as an immunotherapy prognostic biomarker and therapeutic target in advanced non-small cell lung cancer.","authors":"Liyuan Dai, Liling Huang, Lin Li, Le Tang, Yuankai Shi, Xiaohong Han","doi":"10.1186/s12931-025-03275-w","DOIUrl":"10.1186/s12931-025-03275-w","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"214"},"PeriodicalIF":5.8,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144286919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Transcriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis.","authors":"Georgios Divolis, Evgenia Synolaki, Rodoula Tringidou, Argyrios Tzouvelekis, Dimitrios T Boumpas, Panagiotis Skendros, Ioanna-Evdokia Galani","doi":"10.1186/s12931-025-03180-2","DOIUrl":"10.1186/s12931-025-03180-2","url":null,"abstract":"<p><strong>Background: </strong>Coronavirus disease 2019 (COVID-19) is a respiratory disease linked with deregulated immune responses, leading to hyperinflammation, acute respiratory distress syndrome, and pulmonary fibrosis, often with fatal outcomes. Neutrophils play a central role in COVID-19 pathogenesis, with elevated peripheral blood neutrophil counts correlating with disease severity. Despite extensive research, the molecular processes associated with neutrophil hyperactivation in COVID-19 remain elusive.</p><p><strong>Methods: </strong>To investigate the molecular signatures underlying neutrophil-driven pathology, we conducted transcriptome analysis in neutrophils isolated from the peripheral blood of COVID-19 patients versus healthy individuals. To evaluate the specificity of identified neutrophil signatures in COVID-19, we extended our transcriptomic analysis to neutrophils from patients with idiopathic pulmonary fibrosis (IPF), a non-infectious fibrotic lung disease. Additionally, immunofluorescence staining was performed on lung biopsy specimens from IPF patients to validate transcriptomic findings at the tissue level.</p><p><strong>Results: </strong>Our analysis revealed significant transcriptional changes in COVID-19 neutrophils, particularly in pathways involved in immune regulation, inflammation, and antiviral responses. Additionally, pathways associated with autophagy and chromatin remodeling were upregulated, while translation-related processes were suppressed, indicating an increased predisposition for neutrophil extracellular trap (NET) release. This neutrophil transcriptional signature in COVID-19 appears to be associated with the previously reported deregulation of the Activin/Follistatin system in the periphery. Notably, a comparative transcriptomic analysis with neutrophils isolated from IPF patients revealed the induction of substantially overlapping inflammatory processes, suggesting common deregulated responses in COVID-19 and IPF. Consistently, significant NET formation, a hallmark of COVID-19-related inflammation, was observed within lung biopsies from IPF patients.</p><p><strong>Conclusion: </strong>By delineating both shared and disease-specific molecular pathways, our findings validate the critical role of neutrophils in COVID-19 and IPF pathophysiology, highlighting their involvement in balancing the inflammatory response across diverse lung diseases.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"213"},"PeriodicalIF":5.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144276355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mary Njoroge, Gabriela Pimentel Pinheiro, Cinthia Vila Nova Santana, Hajar Ali, Stephanie Hobbs, Santiago Mena-Bucheli, Natalia Romero-Sandoval, Steven Robertson, Charlotte E Rutter, Donna Davoren, Collin Brooks, Jeroen Douwes, Philip J Cooper, Harriet Mpairwe, Camila A Figueiredo, Alvaro A Cruz, Mauricio L Barreto, Neil Pearce, Lucy Pembrey
{"title":"Causes and MEchanisms foR non-atopic Asthma in Children (CAMERA) study: rationale and protocol.","authors":"Mary Njoroge, Gabriela Pimentel Pinheiro, Cinthia Vila Nova Santana, Hajar Ali, Stephanie Hobbs, Santiago Mena-Bucheli, Natalia Romero-Sandoval, Steven Robertson, Charlotte E Rutter, Donna Davoren, Collin Brooks, Jeroen Douwes, Philip J Cooper, Harriet Mpairwe, Camila A Figueiredo, Alvaro A Cruz, Mauricio L Barreto, Neil Pearce, Lucy Pembrey","doi":"10.1186/s12931-025-03279-6","DOIUrl":"10.1186/s12931-025-03279-6","url":null,"abstract":"<p><strong>Background: </strong>The Causes And MEchanisms foR non-atopic Asthma in children (CAMERA) study was designed to investigate risk factors and mechanisms of non-atopic asthma in children and young adults in Brazil, Ecuador, Uganda, and New Zealand. Initial epidemiological analyses using existing datasets identified and compared risk factors for both atopic and non-atopic asthma. The focus of this paper is the protocol for sample collection and analysis of clinical data on possible non-atopic mechanisms.</p><p><strong>Methods: </strong>In each of the four centres, the CAMERA study will enroll 160 participants aged 10-28 years, equally distributed among atopic asthmatics (AA), non-atopic asthmatics (NAA), atopic non-asthmatics and non-atopic non-asthmatics. Participants will be new recruits or returning World ASthma Phenotypes (WASP) study participants. Phase I consists of skin prick tests to define atopy, a general CAMERA questionnaire that covers respiratory and general health to identify asthma cases, followed by an asthma control questionnaire for asthmatics only. Phase II consists of a stress questionnaire and the following clinical assessments: lung function, nasal cytology, blood sampling, in vitro whole blood stimulation to assess IFN-γ production, hair cortisol concentration, dry air and capsaicin challenges, plus in a subset, cold air challenges. Analyses will compare inflammatory, physiological and clinical parameters across the four groups overall and by country.</p><p><strong>Discussion: </strong>Here, we present the protocol for the CAMERA study, to provide relevant methodological details for CAMERA publications and to allow other centres globally to conduct similar analyses. The findings of this mechanistic multi-centre study will inform new and phenotype-specific prevention and treatment approaches.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"212"},"PeriodicalIF":5.8,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12142945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144235690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhigang Chen, Huiying Lu, Ao Liu, Jia Weng, Lei Gan, Lina Zhou, Xiao Ding, Shicheng Li
{"title":"TRANS: a prediction model for EGFR mutation status in NSCLC based on radiomics and clinical features.","authors":"Zhigang Chen, Huiying Lu, Ao Liu, Jia Weng, Lei Gan, Lina Zhou, Xiao Ding, Shicheng Li","doi":"10.1186/s12931-025-03287-6","DOIUrl":"10.1186/s12931-025-03287-6","url":null,"abstract":"<p><strong>Background: </strong>Early detection of epidermal growth factor receptor (EGFR) is critical for guiding therapeutic decisions in non-small-cell lung cancer (NSCLC). The study aims to develop a predictive model for EGFR mutations with multicohort data.</p><p><strong>Methods: </strong>The study enrolled 254 NSCLC patients of four cohorts: the Affiliated Hospital of Qingdao University (AHQU, n = 54), the Second Affiliated Hospital of Soochow University (SAHSU, n = 78), TCGA-NSCLC (n = 91), and CPTAC-NSCLC (n = 31). Radiomic features were extracted using the LIFEx software. The least absolute shrinkage and selection operator (LASSO) algorithm was utilized to select predictive features of CT radiomics, clinical data, and RNA sequencing, which were evaluated using receiver operating characteristic (ROC) curves. A nomogram was developed by integrating predictive features. Biological functions were analyzed utilizing RNA sequencing data.</p><p><strong>Results: </strong>Eight radiomic features, four clinical features, and seven genomic features were selected to construct distinct signatures. Through internal 5-fold cross-validation, the first two signatures demonstrated notable discrimination capabilities for distinguishing between mutated and wild-type EGFR, resulting in area under the curve (AUC) values of 0.79 (± 0.08) and 0.74 (± 0.06), respectively. The combination of clinical variables and radiomics signature resulted in an increased AUC of 0.84 (± 0.01). This combined model was named TRANS, representing TTF-1, radiomic signature, AE1/AE3, NapsinA, and stage, which uses radiomics and routine immunohistochemistry markers as inputs. High-risk TRANS was observed to be associated with poor overall survival, and showed relationships with high T cell infiltration and response to PD-1 immunotherapy.</p><p><strong>Conclusions: </strong>The TRANS model demonstrated favorable ability in predicting EGFR mutation status in NSCLC, providing a valuable approach for optimizing therapeutic strategies in clinical practice.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"211"},"PeriodicalIF":5.8,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144235691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leon Soltész, Judith Leyens, Marieke Vogel, Thomas Muders, Christian Putensen, Florian Kipfmueller, Till Dresbach, Andreas Mueller, Lukas Schroeder
{"title":"Correction: EIT guided evaluation of regional ventilation distributions in neonatal and pediatric ARDS: a prospective feasibility study.","authors":"Leon Soltész, Judith Leyens, Marieke Vogel, Thomas Muders, Christian Putensen, Florian Kipfmueller, Till Dresbach, Andreas Mueller, Lukas Schroeder","doi":"10.1186/s12931-025-03292-9","DOIUrl":"10.1186/s12931-025-03292-9","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"208"},"PeriodicalIF":5.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"HNRNPH1 promotes autophagy to inhibit the development of lung adenocarcinoma via the HSP90AB1/MAP1LC3B axis.","authors":"Rong Li, Fen Li, Qian Liu, Xu Wu, Xiaowu Tan","doi":"10.1186/s12931-025-03280-z","DOIUrl":"10.1186/s12931-025-03280-z","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is a prevalent subtype of lung cancer (LC) whose progression is regulated by multiple genes. This study sought to find the impact and mechanism of HNRNPH1 on LUAD.</p><p><strong>Methods: </strong>The expression and role of HSP90AB1, HNRNPH1, and autophagy-related protein MAP1LC3B in LUAD were detected. Additionally, bioinformatics analysis, silencing and overexpression techniques, and in vivo modeling were used to explore the regulatory mechanisms of these proteins in the progression of LUAD.</p><p><strong>Results: </strong>HSP90AB1 showed high expression in LUAD and was linked to a worse prognosis. Overexpression of HSP90AB1 significantly promoted the malignant phenotype of LUAD cells and inhibited MAP1LC3B-mediated autophagy. However, overexpression of HNRNPH1 could reverse the malignant phenotype resulting from HSP90AB1 overexpression and promote MAP1LC3B-mediated autophagy by binding to HSP90AB1 mRNA and inhibiting its protein expression. Animal experiments also revealed that overexpression of HNRNPH1 could inhibit tumor progression by promoting cellular autophagy.</p><p><strong>Conclusions: </strong>We verified the key role of HSP90AB1, HNRNPH1, and MAP1LC3B in LUAD, and revealed a possible regulatory mechanism, namely, HNRNPH1 could inhibit the development of LUAD by promoting autophagy through the HSP90AB1/MAP1LC3B axis. These findings may offer new insights for improving the treatment and prognosis of LUAD.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"206"},"PeriodicalIF":5.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shanzina Iasmin Sompa, Jie Ji, Mizanur Rahman, Bengt Sjögren, Swapna Upadhyay, Koustav Ganguly, Anna-Carin Olin, Anna Bergström, Lena Palmberg
{"title":"Local and systemic effects in e-cigarette users compared to cigarette smokers, dual users, and non-smokers.","authors":"Shanzina Iasmin Sompa, Jie Ji, Mizanur Rahman, Bengt Sjögren, Swapna Upadhyay, Koustav Ganguly, Anna-Carin Olin, Anna Bergström, Lena Palmberg","doi":"10.1186/s12931-025-03289-4","DOIUrl":"10.1186/s12931-025-03289-4","url":null,"abstract":"<p><strong>Background: </strong>The use of electronic (e)-cigarettes in the long term has been associated with an increased risk of respiratory diseases. Dual use of e-cigarettes and traditional cigarettes may increase these risks even more due to the combined exposure effects of these products. The aim of this study was to investigate the local and systemic effects of e-cigarette use for more than one year and compare them with healthy non-smokers, cigarette smokers, and dual users.</p><p><strong>Methods: </strong>The clinical study was conducted among 22 healthy non-smokers, 20 e-cigarette users, 20 cigarette smokers, and 20 dual users. Participants were matched with age and BMI, had normal baseline lung function, and had no allergies. Exhaled FeNO and bronchial responsiveness were assessed along with reactive oxygen species (ROS), toll-like receptor (TLR) expression, and inflammatory cytokines in blood and sputum.</p><p><strong>Results: </strong>Exhaled FeNO was higher in e-cigarette users (14 ppb, p = 0.04) and lower in cigarette smokers (9 ppb, p = 0.04) compared to healthy non-smokers (11 ppb). Bronchial responsiveness was increased in e-cigarette users (1.9 mg, p = 0.01) and cigarette smokers (1.9 mg, p = 0.01) compared to healthy non-smokers (2.9 mg). ROS in blood and sputum in e-cigarette users (p = 0.005 and p = 0.04) and dual users (p = 0.003 and p = 0.04) were increased. Also, TLR2 expression in blood granulocytes in all exposed groups (p = 0.001), TLR2 and TLR4 expression in sputum in e-cigarette users (p = 0.04 and p = 0.03) and dual users (p < 0.0001 and p = 0.004) were increased. Moreover, the percentage of IL13 and IFNγ cytokine-producing T cells in blood were increased in e-cigarette users (p = 0.0001 and p < 0.0001) and dual users (p = 0.001 and p < 0.0001).</p><p><strong>Conclusion: </strong>Our research indicates that both local and systemic inflammatory responses, along with innate immune receptor activity, were significantly altered in e-cigarette users and dual users. Notably, these alterations were detected in e-cigarette users within a short timeframe of just 1 to 3 years of use.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"207"},"PeriodicalIF":5.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sputum sample quality selection in microbiota research; a chance to improve methods??","authors":"Eleanor Kewin, Ross Langley, Alison Jane Dicker","doi":"10.1186/s12931-025-03286-7","DOIUrl":"10.1186/s12931-025-03286-7","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"210"},"PeriodicalIF":5.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Steven L Taylor, Collin R Brooks, Levi Elms, Sarah K Manning, Alyson Richard, Jeroen Burmanje, Jeroen Douwes, Geraint B Rogers
{"title":"Sputum quality affects assessment of airway microbiology in childhood asthma.","authors":"Steven L Taylor, Collin R Brooks, Levi Elms, Sarah K Manning, Alyson Richard, Jeroen Burmanje, Jeroen Douwes, Geraint B Rogers","doi":"10.1186/s12931-025-03266-x","DOIUrl":"10.1186/s12931-025-03266-x","url":null,"abstract":"<p><strong>Background: </strong>The analysis of sputum is the principal basis for characterising lower airway microbiology in those with chronic respiratory conditions. For such analysis to be informative, samples that poorly reflect the lower airways must be identified and removed. Our cross-sectional study explored the relationship between the quality of sputum samples and their microbiological content. We further investigated the impact of excluding low quality samples on observed microbiota-disease relationships in childhood asthma.</p><p><strong>Methods: </strong>Induced sputum was collected from children with or without asthma. Sputum quality was assessed according to squamous cell%, cell viability%, detection of sputum plugs, and salivary α-amylase levels. Sputum microbiota was characterised by 16S rRNA amplicon sequencing and qPCR.</p><p><strong>Results: </strong>Of 170 participants, 130 had asthma. Between 19% (32/170) and 29% (53/170) of samples were deemed to be of insufficient quality, depending on the quality criterion applied. Stratification of samples based on any of the sputum quality cut-offs resulted in significant differences in microbiota characteristics (all p < 0.05), with salivary α-amylase the least discriminant between microbiota of acceptable and unacceptable samples. The removal of 53 poor-quality samples based on ≥ 30% squamous cells identified a difference in the sputum microbiota by asthma status (p = 0.017) that was not evident otherwise, including significantly higher levels of Haemophilus and Gemella in asthma samples.</p><p><strong>Conclusions: </strong>Upper airway contamination of induced sputum samples from children is common. Exclusion of samples based on ≥ 30% squamous cells enables identification of asthma-airway microbiology relationships that are otherwise not apparent.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"209"},"PeriodicalIF":5.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}