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Journal articleWang M, He Y, Hu H, et al., 2026, , Redox Rep, Vol: 31
BACKGROUND: Fatty acid oxidation (FAO) is implicated in lung diseases, but its role in bronchial asthma is not fully understood. We investigated its effect on airway epithelial barrier integrity. METHODS: Using a house dust mite (HDM)-induced murine asthma model and HDM, IL-4, IL-13, or TNF-α stimulated human primary bronchial epithelial cells (BECs) and bronchial epithelial (Beas-2b) cells, we modulated FAO with L-carnitine (agonist) and Etomoxir (inhibitor). BECs and Beas-2b cells were infected with lentivirus-mediated CPT1A shRNA prior to stimulation. Barrier function, mitochondrial oxidative stress, inflammation, and metabolism were assessed. RESULTS: FAO level in lungs negatively correlated with increased inflammation and tissue injury in HDM-induced asthmatic mice (all p < 0.05), while positively regulating tight junction protein expression. In BECs and Beas-2b cells, Etomoxir treatment and CPT1A knockdown exacerbated the impairment of FAO caused by various stimulants (all p < 0.05). Furthermore, FAO negatively regulated HDM/cytokine-induced epithelial barrier damage, hyperactive inflammatory response, and mitochondrial dysfunction in Beas-2b cells (all p < 0.05). In contrast, treatment with L-carnitine significantly alleviated these pathophysiological features in both in vivo and in vitro models. CONCLUSION: FAO plays a protective role in the occurrence and development of asthma by maintaining airway epithelial cell homeostasis and barrier function.
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Journal articleToumpanakis D, Usmani OS, Wells AU, et al., 2026, , Chest, Vol: 169, ISSN: 0012-3692
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Journal articlePhilip KEJ, Owles H, McVey S, et al., 2026, , The Lancet Digital Health, Pages: 100988-100988, ISSN: 2589-7500
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Journal articleKlimek L, Mullol J, Reitsma S, et al., 2026, , Allergy
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Journal articleAndersson LI, Kupczyk M, Dahl茅n B, et al., 2026, , Allergy
BACKGROUND: Obesity-related asthma (OBA) is a distinct asthma phenotype, with increased severity. Adipokine release from excessive adipose tissue is suggested to be a key feature of OBA pathophysiology. However, it is unclear how the clinical characteristics of severe asthma associate with adipokine mediators. We examined systemic adipokine levels and evaluated relationships with disease severity, weight, sex, and steroid treatment in asthma. METHODS: A multiplex immunoassay for nine adipokines with proposed involvement in obesity-related inflammation (adiponectin, adipsin, BAFF, chemerin, FGF-21, leptin, lipocalin-2/NGAL, osteonectin and resistin) was designed. Plasma adipokines were measured in 127 patients with mild-to-moderate asthma (MMA) or severe asthma (SA) from the European BIOAIR cohort at baseline and after a controlled 2-week oral corticosteroid (OCS) intervention. RESULTS: Leptin and chemerin were significantly increased in patients with SA vs. MMA. Leptin, adiponectin, adipsin, and NGAL were affected by sex, whereas leptin and adipsin were strongly affected by weight. OCS increased leptin and adiponectin, decreased adipsin and BAFF, and did not affect osteonectin, resistin, or chemerin. No adipokines showed positive associations with exhaled NO, blood or sputum eosinophils, although certain correlations with serum CRP, blood, and sputum neutrophils were observed. CONCLUSIONS: Overall, we observe variable relationships between the nine adipokines, obesity and asthma severity. There were no relationships between adipokine levels and type-2 airway inflammation, yet associations with systemic neutrophilic inflammation were seen. Although one adipokine, chemerin, was independently associated with asthma severity, deciphering the role of adipokines in OBA is complex due to the influence of sex, BMI, and OCS.
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Journal articleDevulder JV, Fenwick PS, Kolosionek E, et al., 2026, , Aging Cell, Vol: 25, ISSN: 1474-9718
<jats:title>ABSTRACT</jats:title> <jats:p> Ageing and cellular senescence significantly contribute to the progression of age鈥恟elated diseases, particularly chronic obstructive pulmonary disease (COPD). Cellular senescence refers to the cessation of cell division in response to stress and damage. While senescent cells remain metabolically active, they secrete pro鈥恑nflammatory factors that drive disease progression. Senolytic therapies aim to selectively target and eliminate these senescent cells by inducing their apoptosis. This study examines the senolytic potential of BCL <jats:sub>XL</jats:sub> 鈥怭ROTAC, a novel proteolysis鈥恡argeting chimera designed to degrade BCL <jats:sub>XL</jats:sub> , in small airway epithelial cells and fibroblasts from patients with COPD. Treatment of COPD small airway epithelial cells and fibroblasts with BCL <jats:sub>XL</jats:sub> 鈥怭ROTAC led to their apoptosis through the activation of caspase 3, along with a reduction in senescence markers such as p21 <jats:sup>CIP1</jats:sup> , p16 <jats:sup>INK4a</jats:sup> and senescence鈥恆ssociated β鈥恎alactosidase. The effects of BCL <jats:sub>XL</jats:sub> 鈥怭ROTAC were selective for senescent cells and did not affect non鈥怌OPD cells. The clearance of COPD small airway epithelial cells and fibroblasts by BCL <jats:sub>XL</jats:sub> 鈥怭ROTAC was associated with an increase in the proliferation marker Ki67 and enhanced cell proliferation. Additionally, in precision鈥恈ut lung slices obtained from COPD patients, BCL <jats:sub>XL</jats:sub> 鈥怭ROTAC signific
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Journal articleFreeman A, Rink S, Bansal AT, et al., 2026, , Lancet Reg Health Eur, Vol: 63
BACKGROUND: The phenotypic nature of multimorbidity in severe asthma is poorly understood. Our aims in this study were to define multimorbidity phenotypes and their characteristics in severe asthma across Europe by identifying and characterising co-aggregation of comorbidities. METHODS: Cross-sectional patient data were analysed from the pan-European Severe Heterogenous Asthma 91桃色 Collaboration: Patient Centred (SHARP) Central database of national severe asthma registries. Patients were grouped by four European regions (North, South, East, and West). Hierarchical clustering of comorbidities was applied to characterise the correlation structure of the ten commonest comorbidities within these geographical regions. Subsequent multimorbidity phenotypes (MMP) and their clinical features were then defined. FINDINGS: Data were available for 2690 severe asthma patients and 23 comorbidities from 11 countries. Three comorbidity clusters were consistently seen across the four European regions: 1) osteoporosis plus steroid-induced weight gain, 2) eczema plus rhinitis, and 3) chronic sinusitis plus nasal polyps. Four further comorbidities (obesity, bronchiectasis, gastro-oesophageal reflux disease, psychological factors) showed variable clustering. Multimorbidity was ubiquitous. Patients were assigned multimorbidity phenotypes (MMP) according to comorbidity cluster alignment. MMP sn (sinonasal-associated) and MMP u (no specific cluster alignment) were commonest. MMP ster (steroid-associated multimorbidity) had highest maintenance oral steroid (m-OCS) use, and Body Mass Index, plus worst lung function, asthma control, and asthma exacerbation frequency. MMP max (maximal multimorbidity) showed high prevalence of variably assigned comorbidities, higher m-OCS and biologic treatment needs. INTERPRETATION: Multimorbidity is common in severe asthma and can be classified into replicable novel phenotypes with characteristic clinical traits and outcomes. Recognising these phenotypes c
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Journal articleKarp T, Merid SK, Kermani NZ, et al., 2026, , J Allergy Clin Immunol, Vol: 157, Pages: 879-889
BACKGROUND: Type 2 (T2)-low asthma is defined by low levels of T2 inflammation and is associated with resistance to inhaled corticosteroids. Its molecular mechanisms are mostly unknown, and treatment options are limited. We previously showed that nasal brush transcriptomes differ between asthma and controls, reflecting disease-relevant biology. OBJECTIVE: We explored nasal gene expression related to T2-low asthma in the ATLANTIS cohort. METHODS: We compared nasal brush RNA sequencing data between 82 T2-low and 63 T2-high asthma patients and 57 controls. T2-low asthma was defined as blood eosinophil counts < 0.15 × 109/L and Feno < 25 ppb and T2-high as blood eosinophil counts > 0.3 × 109/L and Feno > 25 ppb. Weighted gene coexpression network analysis (WGCNA) was applied to identify gene modules associated with T2-low asthma. The BAMSE and U-BIOPRED cohorts were used for replication analyses. RESULTS: Although differentially expressed genes were found in patients with T2-high asthma across all 3 cohorts, no differentially expressed genes were observed in individuals with T2-low disease compared to controls in ATLANTIS, nor consistently across other cohorts. Our assessment of molecular heterogeneity could not attribute this result to greater intersample variability within the T2-low group. WGCNA in ATLANTIS identified "black" and "purple" gene modules linked to T2-low asthma, with genes enriched in T-cell immunity and ribosomal RNA biology pathways, respectively. The "black" module was replicated in U-BIOPRED and showed the same direction in BAMSE. CONCLUSION: T2-high asthma shows a distinct nasal gene expression signature compared to healthy controls, while patients with T2-low asthma exhibit no consistent changes. Future studies should explore T-cell immunity in T2-low asthma and integrate lower airway multiomics data.
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Journal articleWawman RE, Shah PL, Boffito M, et al., 2026, , ERJ Open 91桃色, ISSN: 2312-0541
Question addressed by the studyFavipiravir has shown efficacy against SARS-CoV-2 in patients under 60, but data linking plasma concentrations to clinical outcomes are limited. This study investigated whether favipiravir plasma concentrations influence clinical efficacy and outcomes in hospitalised COVID-19 patients and asked: how can antiviral dosing strategies be optimised to improve pandemic preparedness and treatment efficacy?Materials/patients and methodsAdult participants were drawn from the PIONEER trial, in which patients received oral favipiravir (1800鈥卪g twice daily on day 1, then 800鈥卪g twice daily for nine days) plus standard care. This analysis included patients with confirmed COVID-19 and ≥75% study adherence. Samples were collected between days 5–10 post-treatment initiation. The primary outcome was time to clinical improvement. Secondary outcomes included achievement of clinical improvement and mortality risk.ResultsOf 140 patients (50% male; mean age 59.5 [sd 14.8]), 29 (21%) reached target plasma concentrations. Mean time to improvement was 7.7 [5.9] vs 9.1 [7.2] days for target achievers vs non-achievers (p=0.26). Target was more often achieved in females (34%) than males (7%) (p=0.0002). Plasma concentration inversely correlated with BMI (r=–0.4; p<0.0001), with lower BMI in achievers (26.0 [5.1] vs 30.5 [6.9]; p=0.003). ALP and ALT levels were also lower in achievers (p=0.004 and p=0.02, respectively).Answer to the questionMost patients did not reach target favipiravir levels. Concentrations were influenced by sex, BMI, and liver function, confirming the need for pharmacokinetically guided dosing and therapeutic monitoring to optimise antiviral efficacy in future pandemic responses.
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Journal articleDevulder J, Fenwick P, Kolosionek E, et al., 2026,
Clearance of senescent cells by BCLXL-PROTAC: a novel approach to treat COPD?
, Aging Cell, ISSN: 1474-9718Aging and cellular senescence significantly contribute to the progression of age-related diseases, particularly chronic obstructive pulmonary disease (COPD). Cellular senescence refers to the cessation of cell division in response to stress and damage. While senescent cells remain metabolically active, they secrete pro-inflammatory factors that drive disease progression. Senolytic therapies aim to selectively target and eliminate these senescent cells by inducing their apoptosis. This study examines the senolytic potential of BCLXL-PROTAC, a novel proteolysis-targeting chimera designed to degrade BCLXL, in small airway epithelial cells and fibroblasts from patients with COPD. Treatment of COPD small airway epithelial cells and fibroblasts with BCLXL-PROTAC led to their apoptosis through the activation of caspase 3, along with a reduction in senescence markers such as p21CIP1, p16INK4a, and senescence-associated β galactosidase. The effects of BCLXL-PROTAC were selective for senescent cells and did not affect non-COPD cells. The clearance of COPD small airway epithelial cells and fibroblasts by BCLXL-PROTAC was associated with an increase in the proliferation marker Ki67 and enhanced cell proliferation. Additionally, in precision-cut lung slices obtained from COPD patients, BCLXL-PROTAC significantly reduced p21CIP1 expression in the airway epithelium, validating its effectiveness in a more complex tissue environment. These findings demonstrate that BCLXL-PROTAC is a potent and selective senolytic agent that may promote lung cell rejuvenation, supporting its potential as a novel therapeutic strategy for age-related diseases, including COPD.
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Journal articleXie M, Chang Q, Li C, et al., 2026, , Environ Pollut, Vol: 393
Ambient ozone (O3), a ubiquitous oxidant gas and key component of photochemical smog, damages the airway epithelium, provokes oxidative stress, and sustains chronic inflammation, which favors the onset and advancement of chronic obstructive pulmonary disease (COPD). Yet the molecular sensors linking long-term ozone exposure to COPD remain incompletely defined. We examined whether the oxidant-sensitive channel Transient receptor potential ankyrin 1 (TRPA1) mediates ozone-driven murine model of COPD through the Wnt5a/GSK3β/β-catenin pathway. C57BL/6J or TRPA1-deficient mice underwent ozone exposure (2.5 ppm, 3 h/session) every 3 days for 2 months, following administration of either the TRPA1 antagonist A967079 or the Wnt5a/GSK3β/β-catenin inhibitor XAV-939. Similarly, BEAS-2B cells treated with A967079 or XAV-939 or TRPA1-silenced cells were subjected to ozone (1 ppm, 3 h/day) for 4 consecutive days. Oxidative stress, inflammatory responses, emphysematous changes, mitochondrial dysfunction, and airway remodeling were assessed. In addition, gene set variation analysis (GSVA) was used to quantify Reactome Wnt5a/GSK3β/β-catenin pathway activity through public COPD transcriptomic cohorts. Pharmacological inhibition or genetic deficiency of TRPA1 significantly attenuated ozone-induced lung function impairment, and ozone-triggered oxidative stress, emphysematous changes, mitochondrial dysfunction, and airway remodeling. Notably, pharmacological suppression of the Wnt5a/GSK3β/β-catenin pathway using XAV-939 produced comparable protective effects to TRPA1 blockade in both ozone-exposed murine models and BEAS-2B cells. GSVA demonstrated tissue-specific associations between TRPA1 and Wnt5a/GSK3β/β-catenin pathway in COPD patients. TRPA1 mediates crucially ozone-induced COPD through modulation of the Wnt5a/GSK-3β/β-catenin signaling. Therapeutic targeting of both TRPA1 and Wnt5a/GSK3β/β-cat
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Journal articleDinh C-T, Lee Y-L, Chang L-T, et al., 2026, , Expert Rev Hematol, Pages: 1-10
INTRODUCTION: Air pollution and household fuel use may impair hematologic health through inflammation and oxidative stress. We synthesized evidence on associations of ambient/household air pollution with anemia risk and erythrocyte indices. METHODS: We searched PubMed, Embase, and Web of Science (inception-27 September 2025). Two reviewers independently screened and extracted data, and assessed risk of bias using Joanna Briggs Institute checklists. Random-effects meta-analyses pooled risk ratios (RRs) per 10 µg/m3 for particulate matter with aerodynamic diameter ≤10 µm (PM10), ≤2.5 µm (PM2.5), and nitrogen dioxide (NO2), and by household fuel type. RESULTS: Thirty-six studies were included. Each 10 µg/m3 increase in PM2.5 and NO2 was associated with higher anemia risk (RR 1.200, 95% CI 1.041-1.384, I2 98.2%; RR 1.127, 95% CI 1.025-1.241, I2 98.0%). Solid and biomass fuel increased anemia risk (RR 1.143, 95% CI 1.027-1.274, I2 82.9%; RR 1.271, 95% CI 1.050-1.539, I2 91.7%). PM10 was associated with lower hemoglobin (0.074 g/dL, 95% CI -0.124 to -0.023, I2 90.7%). Effects were generally stronger in males and in low- and middle-income countries. CONCLUSIONS: Ambient and household air pollution are associated with increased anemia risk and reductions in hemoglobin; high heterogeneity and observational designs limit causal inference.
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Journal articleWen H, Kole T, Carpaij OA, et al., 2026, , Allergy
BACKGROUND: Transcriptomic analysis of bronchial brushes reveals asthma-associated gene signatures but is limited by the invasiveness of bronchoscopy. Based on the "united airways" hypothesis, we evaluated whether and to what extent nasal brushes reflect asthma-associated transcriptomic changes in the lower airways. METHODS: In the ARMS study, we included 26 asthma patients and 28 healthy controls, all fully clinically characterized. Nasal and bronchial brushes were collected for RNA sequencing. We used edgeR and WGCNA to identify asthma-associated genes and modules in bronchial brushes. We assessed their expression patterns in ARMS nasal brushes and validated the findings in the independent ATLANTIS study (n = 427). RESULTS: We identified 51 asthma-associated genes in the lower airways, of which 40 were up-regulated and 11 were down-regulated in asthma compared to healthy controls. Seven of the 40 up-regulated genes were also up-regulated in ARMS nasal brushes and validated in ATLANTIS: CLCA1, FETUB, CST1, NTRK2, CDH26, TPSAB1, and DHX35. WGCNA revealed two modules that were consistently elevated in asthma across bronchial and nasal brushes in ARMS and confirmed in ATLANTIS. One module represents IL-13 related inflammation, whereas the other represents mast cell activity. CONCLUSION: The asthma-associated gene signatures of the lower and upper airways show a limited but biologically coherent overlap, with seven genes and two gene modules consistently elevated in asthma. The shared gene signatures reflect two separate components of type 2 inflammation: IL-13 related inflammation and mast cell activity. Selected nasal gene signatures offer a non-invasive tool to identify asthma endotypes with distinct molecular mechanisms driving underlying disease biology.
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Journal articleXie M, Weng J, Li C, et al., 2026, , Lung, Vol: 204
BACKGROUND: Ozone (O鈧) exposure induces acute airway injury characterized by airway hyperresponsiveness (AHR) and airway mucus hypersecretion (AMH). Oxidative stress and mitochondria-derived reactive oxygen species (mtROS) are key contributors. We investigated and compared the protective mechanisms of N-acetylcysteine (NAC) and the mitochondria-targeted antioxidant Elamipretide (SS-31) in O鈧-induced airway inflammation, AHR and AMH. METHODS: Wild-type C57BL/6J mice received intraperitoneal NAC or SS-31 1 h before a single O鈧 exposure. AHR, bronchoalveolar lavage (BAL) inflammatory cells, mucus production and mucin expression, inflammatory mediators, oxidative stress indices, and PI3K/AKT and NLRP3/caspase-1/GSDMD pathway activation were assessed in vivo. BEAS-2B cells were pretreated with NAC, SS-31, or the PI3K/AKT inhibitor LY294002 before O鈧 exposure, and pathway activation was evaluate d in vitro. RESULTS: NAC and SS-31 comparably attenuated O鈧-induced AHR, reduced BAL inflammatory cell influx, and decreased AMH and MUC5B expression. Both treatments improved redox balance by reducing ROS/mtROS, lowering malondialdehyde (MDA), increasing superoxide dismutase (SOD) activity, and improving GSH/GSSG. NAC and SS-31 also suppressed O鈧-induced inflammatory gene expression and inhibited activation of PI3K/AKT and NLRP3/caspase-1/GSDMD signaling in mouse lungs and BEAS-2B cells. PI3K inhibition recapitulated these protective effects in vitro, supporting a mechanistic role for PI3K/AKT signaling during acute O鈧 exposure. CONCLUSIONS: NAC and SS-31 protect against acute O鈧-induced AHR and AMH by alleviating oxidative stress and suppressing PI3K/AKT-driven inflammatory and pyroptotic pathways. Targeting oxidative stress, including mitochondrial ROS, may represent a viable strategy to mitigate airway damage caused by acute O鈧 exposure.
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Journal articleCarlsten C, Salvi S, Wong GWK, et al., 2026, , ERJ Open 91桃色, Pages: 01127-2025
<jats:p>Air pollution is a major threat to respiratory health. We review the current literature on accessible interventions that could help patients build resilience against this threat. We explore the potential benefits of antioxidant-rich diets, including supplements such as fish oil, vitamins C, D, E and prebiotics, which have shown promise in reducing inflammation and oxidative stress, thereby mitigating air pollution-related respiratory decline. Nasal washes are commonly used to clear nasal passages, which could support may aid to clearing pollutants from the nasal passages and improve mucociliary clearance. Furthermore, medications such as nonsteroidal anti-inflammatory drugs and intranasal corticosteroids may have been reported to reduce pollutant- related airway inflammation and lung function deterioration triggered by pollutant exposure. Given the generally favourable safety profile of these interventions, they are reasonable to consider in consultation with a care provider. Further research is needed to establish optimal dosing, safety and long-term efficacy, particularly for those exposed to chronic air pollution. Healthcare professionals should work together to further identify and implement effective interventions to mitigate the impact of air pollution on respiratory health.</jats:p>
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Journal articleLee B, Anpalagan H, Wong E, et al., 2026,
Hormone replacement therapy and the risk of asthma attacks: population-based cohort study
, ERJ Open 91桃色, ISSN: 2312-0541Background Women experience higher rates and greater severity of asthma after puberty, suggesting that sex hormones play a key role in airway disease. Hormone replacement therapy (HRT), which acutely alters circulating sex hormone levels, provides a useful model to examine their effects on asthma attacks. We sought to examine the association between HRT use and asthma attacks. Methods We obtained a cohort of women with asthma, aged 45 to 60 years, using nationwide U.K. primary care health records linked to hospital and mortality data, 2004-2020, to compare HRT-users to non-users. We applied inverse-probability of treatment weighting and Cox proportional hazards, accounting for demographics, asthma severity and comorbidities; stratifying by potential modifiers: body mass index (BMI), blood eosinophil count, smoking and HRT-type (oestrogen-only, progesterone-only and combined). Results 182,010 women were eligible for the study, of whom 9,663 were incident HRT users and 172,347 were non-users. Median age was 52 years (IQR: 50-55 years). HRT-users and non-users were broadly similar in terms of BMI, smoking history but non-users had slightly higher proportions residing in more deprived areas, with more comorbidities, higher reliever use and asthma attacks in the year before study entry, but lower use of preventer inhalers. After applying weighting, there was no association found between HRT use and asthma attacks (weighted-HR 0.97, 95% CI 0.90-1.04). There was no modification of that association by blood eosinophil level, BMI, smoking history or HRT-type. Conclusion Hormone replacement therapy use is not associated with asthma attacks in women with established asthma aged 45 to 60 years old.
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Journal articleAlimohammadi M, Tahmasebi S, Amani D, et al., 2026, , Int Immunopharmacol, Vol: 172
BACKGROUND: MiR-146a has been found to be a tumor suppressor and is downregulated in NSCLC cells. This study investigated the effects of delivering miR-146a via tumor-derived exosomes (TEX-MiR-146a) on the behavior of malignant cells and immunological modulation in NSCLC models. METHODS: miR-146a expression was evaluated in A-549 and normal MRC-5 lung epithelial cells. Exosomes were isolated from A-549 cells, loaded with a miR-146a mimic, and characterized for size, morphology, surface markers, and loading efficiency. In vitro, the functional effects of TEXmiR-146a were compared to controls using tests for cell survival, apoptosis, migration, invasion, wound healing, colony formation, and gene expression. Co-culture immunological assays, including T cell subset and cytokine profiling, were also performed using patient-derived peripheral blood mononuclear cells (PBMCs). RESULTS: TEXmiR-146a efficiently loaded miR-146a into cells (60.1 % ± 4.0 efficiency, P < 0.0001). Treatment with TEXmiR-146a (25 μg/ml) significantly reduced the viability of A-549 cells by ∼51 % after 48 h (P < 0.0001). Cell migration and invasion were inhibited by >50 %, with migrating cells reduced to 116.7 ± 7.09 (P < 0.001) and invading cells to 171.7 ± 6.028 (P < 0.001), respectively, compared to controls. Pro-apoptotic genes Bax/Bcl-2 (P = 0.0002) and Caspase-3 were upregulated (P = 0.0003), while metastatic and immunoregulatory genes VEGF-A, MMP-9, STAT3, MYD88, and PD-L1 were downregulated (all P < 0.05). In patient PBMCs, TEXmiR-146a increased the frequency of cytotoxic CD8+ T cells (24.75 ± 1.23 % versus 20.15 ± 1.26 %, P < 0.0001) and decreased Treg cells (2.01 ± 1.22 % versus 4.04 ± 1.72 %, P = 0.015) compared to th
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Journal articleAnanth S, Wedzicha JA, 2026, , PRESSE MEDICALE, Vol: 55, ISSN: 0755-4982
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Journal articleMao R, Zhang H, Chang Q, et al., 2026, , Chin Med J Pulm Crit Care Med, Vol: 4, Pages: 81-91
BACKGROUND: Interstitial lung abnormalities (ILAs) are incidental abnormal lung findings on computed tomography that can co-exist with lung cancer, but risk factors for their progression and impact on survival after lung cancer resection remain unclear. This study aimed to identify risk factors for ILA progression, develop a radiomics-based model to predict it, and evaluate the association between ILA progression and mortality. METHODS: Patients with ILAs who underwent lung cancer resection in Shanghai Chest Hospital between January 2016 and May 2019 were retrospectively selected and divided into three subcategories at baseline: non-subpleural ILAs, subpleural non-fibrotic ILAs, and subpleural fibrotic ILAs; and three subcategories during follow-up: improved ILAs, unchanged ILAs, and progressive ILAs. Multivariate logistic regression was used to identify clinical and laboratory risk factors associated with ILA progression, and radiomics-based machine learning models were independently constructed to predict ILA progression using baseline CT imaging features. Survival data were analyzed using Kaplan-Meier curves and Cox proportional hazards regression. RESULTS: There were 1363 ILA cases among 10,295 patients who underwent primary lung cancer resection, with a proportion of 13.24%. After 2- and 4-year follow-up, the progression rates of ILAs were 9.86% (65/659) and 10.19% (43/422), respectively. Subpleural fibrotic ILAs (2-year follow-up: OR鈥=鈥6.078, 95% confidence interval [CI]: 2.633-14.028, P鈥<鈥0.001; 4-year follow-up: OR鈥=鈥3.339, 95% CI: 1.085-10.272, P鈥=鈥0.035), and radiotherapy (OR鈥=鈥13.595, 95% CI: 4.540-40.710, P鈥<鈥0.001; OR鈥=鈥11.496, 95% CI: 2.864-46.141, P鈥=鈥0.001) were risk factors for ILA progression. Using radiomics features extracted from baseline CT, the AutoGluon machine learning model demonstrated high performance in predicting ILA progression among patients with confirmed ILAs (for all ILAs, mean area under curve value: 0.790, accuracy: 0.801 &
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Journal articleXuan S, Wu Y, Liu F, et al., 2026, , Adv Sci (Weinh), Vol: 13
Emphysema remains a major challenge in the management of chronic obstructive pulmonary disease (COPD). This study identifies CD207-positive dendritic cells (CD207+ DCs) as pivotal mediators of emphysema progression. In patients with COPD, the abundance of CD207+ DCs in small airways correlates with both emphysema severity and lung function decline (FEV1%pred). In a murine emphysema model, adoptive transfer of CD207+ DCs reversed the attenuation of emphysema, inflammation and CD8+ T-cell expansion in CD207-knockout mice. Mechanistically, cigarette smoke-induced epithelial GM-CSF drives the expansion of CD207+ DCs. Upon activation by damage-associated molecular patterns (DAMPs), these DCs promote CD8+ T cell proliferation and activation via Birbeck granule-mediated MHC-I antigen cross-presentation. Collectively, these findings demonstrate that CD207+ DCs orchestrate a pathogenic CD8+ T-cell response in emphysema and represent a promising therapeutic target.
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