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Journal articleYin X, Meng J, Durham SR, et al., 2026,
East Meets West in Allergic Airway Disease: Insights From the EAACI Hong Kong Allergy School 2025.
, Allergy, Vol: 81, Pages: 1327-1330 -
Journal articleLai K, Xu T, Chen P, et al., 2026,
Characteristics and management of asthma from the China Asthma Data Registry Project.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541BACKGROUND: There is limited information available on patients with asthma in hospitals in China. We investigated their clinical and phenotypic characteristics and management. METHODS: The China Asthma Data Registry Project (CHART) study is a multicentre, hospital-based, prospective, observational study in which patients were recruited from outpatient clinics. This analysis used baseline cross-sectional data from patients with asthma (≥12 years) enrolled at 58 tertiary hospitals in China between 25 March 2018 and 11 July 2019. RESULTS: A total of 20 683 patients with asthma (56.2% female, 15.0% patients with active tobacco use) were enrolled. Overall, 22.8% had uncontrolled asthma, 39.5% had partially controlled asthma. Furthermore, 45.3% experienced ≥1 exacerbation annually, including 31.7% who required hospitalisation, with only 21.4% having previously used inhaled corticosteroids (ICSs) in the past year. Cough (80.0%) was the most common symptom, followed by wheezing (70.7%), with 14.6% having cough-predominant asthma and 11.4% having cough-variant asthma. Multivariate logistic regression revealed that cough severity independently predicted poor control, irrespective of airflow limitation or inflammatory status. The association was stronger in ICS users than in nonusers across all cough severity metrics: a visual analogue scale (VAS) score ≥40 (aOR 3.88-5.47 versus 2.49-2.94), a cough evaluation test (CET) score ≥12 (aOR 11.15-20.91 versus 3.97-5.55), and a Leicester Cough Questionnaire (LCQ) score <15 (aOR 6.15-13.66 versus 2.45-3.18). CONCLUSIONS: We found significant suboptimal control, a high prevalence of cough-related phenotypes, frequent exacerbations and hospital admissions in patients with asthma attending hospitals. This underscores the need to prioritise the assessment and treatment of cough in asthma.
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Journal articleFu H, Sun P, Yuan X, et al., 2026,
Epithelial-Associated CD207+ DCs Link Allergen Sensing and IL-25-Driven Th2 Inflammation in Asthma.
, Allergy, Vol: 81, Pages: 1522-1535BACKGROUND: IL-25 is a key epithelial-derived alarmin associated with T2-high asthma, yet its downstream mechanisms remain poorly defined. CD207 (Langerin)+ dendritic cells (DCs) are localized at the airway epithelial interface. However, whether these cells respond to epithelial-derived cytokines and contribute to the Th2 immune response in asthma remains unclear. METHODS: Single-cell RNA-seq from healthy human lungs was analyzed to define the transcriptomic features of CD207+ DCs. Their function was validated in a house dust mite (HDM)-induced asthma model using Cd207-/- mice. Flow cytometry was performed on lung and mediastinal lymph nodes. DC-T cell co-cultures were used to assess Th2 polarization. Epithelial-DC interactions were evaluated using transwell co-culture with ALI-differentiated tracheal epithelial cells. Clinical relevance was examined in airway samples from asthma patients in the U-BIOPRED cohort. RESULTS: CD207+ DCs were enriched in intraepithelial compartments and exhibited increased MHC-II and Claudin-1 expression. In asthma, their abundance correlated with T2 signatures and Th2 markers (CRTH2, ST2). CD207 deletion reduced HDM uptake, Th2 cytokines, airway inflammation, and Th2 differentiation. IL-25 induced CD207+ DCs and enhanced their Th2-polarizing capacity in vitro. An IL-25-CD207 co-expression score correlated with IL-4/IL-5/IL-13 levels and was higher in steroid-naïve patients with severe asthma. CONCLUSION: Our study identifies CD207+ DCs as epithelial-associated antigen-presenting cells that bridge IL-25 signaling and Th2 polarization in allergic asthma. Targeting the IL-25-CD207 axis may offer therapeutic opportunities for T2-high asthma.
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Journal articleWilliams TJ, Kermani NZ, Gonzales-Huerta LE, et al., 2026,
A Role for Non-Canonical Caspases in Fungal Allergic Airway Disease.
, Clin Exp Allergy, Vol: 56, Pages: 576-578Inhibition of the murine ortholog caspase‐11 reduces neutrophilia and inflammatory cytokine levels. Wedelolactone or its derivatives offer a potential therapeutic approach for mixed or steroid‐resistant inflammation in allergic fungal airway disease.
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Journal articleToumpanakis D, Usmani OS, Wells AU, et al., 2026,
Response.
, Chest, Vol: 169 -
Journal articleJenkins RG, 2026,
Developing a vaccine strategy to prevent the progression of pulmonary fibrosis.
, Nat Immunol, Vol: 27, Pages: 890-891 -
Journal articleMarques-Mejias A, Bartha I, Ciaccio CE, et al., 2026,
Corrigendum to 'Skin as the target for allergy prevention and treatment' [Annals of Allergy, Asthma & Immunology, Volume 133, Issue 2 (2024) 133-143].
, Ann Allergy Asthma Immunol, Vol: 136 -
Journal articleWallace DV, Hossny EM, Levin M, et al., 2026,
Anaphylaxis Guidelines.
, Immunol Allergy Clin North Am, Vol: 46, Pages: 233-256This article compares 12 national and international anaphylaxis guidelines published between 2006 and 2025, highlighting evolving methodological frameworks, diagnostic criteria, and treatment approaches. While consensus supports prompt epinephrine use, differences remain in definitions, risk stratification, and post-acute care. Gaps in education, early childhood care protocols, and global harmonization continue to exist. The analysis emphasizes the shift from crisis-based to proactive anaphylaxis management and underscores the need for equity-focused, evidence-based interventions.
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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 Research, Pages: 01599-2025, 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 articleLiao Z-A, Tsao P-N, Chen C-M, et al., 2026,
Hippo signaling pathway regulates branching morphogenesis of the fetal lung under hypoxia.
, Pediatr ResBACKGROUND: Hypoxia is known to disrupt embryonic organogenesis and increase the risk of neonatal respiratory disorders. The Hippo pathway is crucial in regulating organ development, size, and cell proliferation. However, the mechanism of how hypoxia affects lung development through this pathway remains unclear. METHODS: Fetal lungs were dissected from embryonic day 11.5 ICR mice and cultured ex vivo under normoxic (21% O₂) or hypoxic (1% O₂) conditions for 72 h, while human fetal lung fibroblasts (IMR-90) were exposed for 24 h. RNA sequencing analysis was performed on mouse fetal lungs. Biochemical analyses of lactate dehydrogenase and interleukin-6 were performed on supernatants. Expression levels of Hippo pathway-related proteins were determined by Western blot and immunofluorescence. RESULTS: Hypoxia markedly inhibited branching morphogenesis, reducing terminal bronchioles and total lung area (p < 0.05). Elevated LDH and IL-6 levels indicated cytotoxicity and inflammation. Western blot analysis revealed increased phosphorylation of YAP/TAZ, accompanied by decreased SOX2 expression (p < 0.05). Furthermore, genes related to cell differentiation and adhesion were also downregulated, indicating disrupted epithelial-mesenchymal coordination. CONCLUSION: These findings suggest that hypoxia may alter Hippo signaling in fetal lung fibroblasts, thereby impairing branching morphogenesis. Prenatal hypoxia exposure might contribute to abnormal lung development and increase susceptibility to neonatal pulmonary disorders. IMPACT: Prenatal hypoxia impairs fetal lung branching morphogenesis by modulating Hippo signaling and fibroblast-derived factors. Prenatal hypoxia enhances cytotoxicity and inflammatory cytokine production in fetal lungs and fibroblasts. This study provides new insights into the pathogenesis of hypoxia-related neonatal lung disorders and suggests Hippo signaling as a potential therapeutic target.
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Journal articleFarias A, Bridgeman VL, Rodrigues FS, et al., 2026,
Type I interferons induced upon respiratory viral infection impair lung metastatic initiation
, Proceedings of the National Academy of Sciences, Vol: 123, ISSN: 0027-8424Metastatic breast cancer accounts for 7% of cancer-related deaths, with the lungs being a common site of cancer spread. In parallel, lower respiratory tract infections, including those caused by respiratory syncytial virus (RSV), remain a common cause of morbidity and mortality worldwide. Acute viral respiratory infections induce marked changes in the lung. However, how these changes influence metastasis initiation and cancer progression remains unclear. Using breast cancer and other cancer cell types in an experimental lung metastasis model, we show that RSV infection impairs tumor cell seeding and early growth in the lung, resulting in fewer metastatic nodules. We demonstrate that restriction of metastatic spread is due to alterations in the lung environment mediated by RSV-induced type I interferons (IFNs). Consistent with this idea, intranasal administration of recombinant IFN-α is sufficient to recapitulate the anti-metastatic effect of RSV infection. Using single cell RNA sequencing supported by in vivo and ex vivo validation, we show that IFN-α influences interactions between epithelial/endothelial cells and cancer cells. Furthermore, both RSV infection and IFN-α administration trigger marked local and systemic upregulation of Galectin-9, an IFN-inducible protein associated with acute respiratory infection in humans. Treatment of cancer cells with Galectin-9 alone is sufficient to restrict metastatic seeding. Altogether, our results suggest that type I IFNs induced by respiratory virus infection render the lungs less permissive to cancer cell seeding and consequently interfere with the ability of tumor cells to successfully initiate metastatic colonization.
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Journal articleSafavi S, Smith S, Jahnke N, et al., 2026,
Lung transplant in people with cystic fibrosis and nontuberculous mycobacteria infection.
, Cochrane Database Syst Rev, Vol: 4RATIONALE: Cystic fibrosis (CF) is an inherited multi-organ disorder. People with CF (pwCF) experience recurrent and chronic lung infections and a progressive loss of lung function. PwCF with poor and rapidly declining lung function may be considered for lung transplantation (LTx), which may improve their quality of life and survival. Nontuberculous mycobacteria (NTM) can cause pulmonary disease in pwCF, and NTM infection is a poor prognostic factor in LTx. Guidelines recommend NTM infection should not automatically preclude LTx. It is important to evaluate the evidence base for LTx in pwCF and NTM pulmonary disease. OBJECTIVES: To evaluate clinical outcomes in pwCF and with NTM infection (NTM infection alone or with NTM pulmonary disease) who undergo LTx by comparing: 1. pwCF with current NTM lung infection who undergo LTx versus those with NTM infection who do not undergo LTX; 2. pwCF with current NTM lung infection who undergo LTx versus those without NTM undergoing LTx. SEARCH METHODS: We searched the Cochrane Cystic Fibrosis Trials Register, CENTRAL, MEDLINE, Embase, and PubMed as well as two ongoing trials registries. We checked references. The latest search date was 17 February 2026. ELIGIBILITY CRITERIA: We considered non-randomised studies of pwCF (any age) with or without NTM lung infection or disease being considered for LTx as well as studies of pwCF and NTM who either did or did not undergo LTx. OUTCOMES: Our critical outcomes were mortality, disseminated NTM infection post-LTx, time to chronic lung allograft dysfunction (CLAD), and quality of life at any time points reported. We additionally planned to report lung function, hospitalisations for pulmonary exacerbations, and nutritional parameters in the review. RISK OF BIAS: We assessed the risk of bias in three studies using ROBINS-I and in one study using the Joanna Briggs Institute checklist for case series. SYNTHESIS METHODS: We could only report results narratively. We used GRADE to assess the cert
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Journal articleMakuyana N, Seldeslachts L, Michiels L, et al., 2026,
Gene delivery of immunomodulatory cytokines to the lung preserves respiratory function during inflammatory challenge.
, Sci Immunol, Vol: 11Respiratory infections that result in severe and life-threatening immune-mediated respiratory decline are a major public health issue. Controlling local respiratory immune reactions without the use of systemic immunosuppressants remains an unmet clinical challenge. We developed a gene delivery system to express anti-inflammatory cytokines in the lung, which reestablishes local immune homeostasis without triggering systemic effects. Using an adeno-associated vector cargo system (AAV6.2-CC10), we induced production of interleukin-2 (IL-2), IL-1 receptor antagonist (IL-1RA), and IL-10 in situ in the lung microenvironment, with no detectable expression or immunological deviation in the peripheral immune system. We demonstrate the effective potential of IL-2, IL-1RA, and IL-10 as immunomodulatory cargos in severe infectious challenge, which reduced respiratory pathology after influenza-associated pulmonary aspergillosis. Thus, the AAV6.2-CC10 platform enables targeted delivery of biologics to the lung, modulates the lung environment, and improves pathology without inducing systemic immune reactions.
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Journal articleMohammed Abdul Wajid L, Saglani S, Nagakumar P, et al., 2026,
Exploring health professional views of management for preschool wheeze: a qualitative study.
, Arch Dis Child, Vol: 111, Pages: 444-448OBJECTIVE: This study aimed to explore health professionals' perspectives on the management of preschool wheeze, including their views on using tests to guide treatment for children with recurrent wheeze. DESIGN: Purposive and snowball sampling were used in this qualitative study to recruit health professionals with experience of managing children with pre-school wheeze from primary and secondary care settings across England. Semi-structured interviews were conducted via Microsoft Teams. Transcripts were analysed thematically, supported by the use of NVivo software, to identify key themes. RESULTS: 14 health professionals participated: four general practitioners, four general paediatricians, four hospital asthma nurses, one tertiary respiratory paediatrician and one primary care nurse. Participants agreed that preschool wheeze remains a significant disease. Thematic analysis identified four key themes: (1) challenges with diagnostic terminology, where a lack of consistent terminology was considered to impact communication and management; (2) diagnostic uncertainty, where the absence of objective tests for early asthma diagnosis negatively contributed to management plans; (3) current practice of investigating children with preschool wheeze, where participants described a lack of infrastructure and approach to performing tests in primary and secondary care; and (4) treatment considerations in which parents' medication beliefs were thought to influence adherence to prescribed treatments. There were differences in the views regarding the management of preschool wheeze between primary and secondary care professionals. CONCLUSION: Health professionals' views highlight inconsistent use of diagnostic terminology for preschool wheeze, contributing to variation in management. Integrated care pathways and infrastructure are urgently needed to improve outcomes for children with preschool wheeze.
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Journal articleKaenmuang P, Barnett JL, Maher TM, et al., 2026,
Association of bronchoalveolar lavage cellular analysis and radiological findings in fibrotic interstitial lung diseases
, BMJ Open Respiratory Research, Vol: 13, ISSN: 2052-4439Background and aims Inflammation may play a role in driving interstitial lung diseases (ILD). Radiological ground-glass opacity (GGO) may not reliably distinguish fine intralobular fibrosis from inflammatory processes in fibrotic ILD. We therefore investigated the relationship between GGO, fibrosis and leukocytes in bronchoalveolar lavage (BAL).Methods We recruited patients with fibrotic ILD at a single centre between May 2014 and February 2018. The extent of GGO and fibrosis was evaluated by two radiologists. Linear regression examined the association between leucocyte numbers in BAL obtained from the right middle lobe and GGO/fibrosis extent in whole lung, adjusting for age, sex and smoking. A Z-test was used to compare the association between BAL and GGO/fibrosis.Results 316 patients were included. Adjusting analyses for covariates, only BAL eosinophil and eosinophil-to-macrophage ratio were positively associated with GGO involvement (0.23 (95% CI 0.03 to 0.42) p=0.023 and 11.21 (95% CI 1.33 to 21.08) p=0.026). Lymphocyte percentages (fibrosis −0.17 vs GGO −0.02 p=0.046); neutrophil percentages (fibrosis 0.38 vs GGO 0.06 p=0.002); neutrophil-to-lymphocyte ratio (fibrosis 0.63 vs GGO −0.05 p=0.027); neutrophil-to-macrophage ratio (fibrosis 14.08 vs GGO 2.57 p=0.015) and neutrophilia (fibrosis 6.81 vs GGO −0.31 p=0.002) all demonstrated a significantly stronger association with fibrosis than GGO.Conclusions Lack of relationships between radiological GGO and BAL leucocyte counts in fibrotic lung disease indicates that GGO may not always be inflammatory in nature. Higher levels of neutrophils were associated with more extensive fibrosis.
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Journal articleWu Z, Yazbeck L, Smith DJF, et al., 2026,
Characterizing Cough and Its Response to Therapy in Hypersensitivity Pneumonitis.
, ChestBACKGROUND: Hypersensitivity pneumonitis (HP) is an immune-mediated interstitial lung disease driven by repeated antigen exposure in susceptible individuals. Cough is a prominent but poorly characterized symptom, especially in relationship to objective measures and treatment response. RESEARCH QUESTION: What are the clinical predictors of cough severity in HP, and how does cough respond to corticosteroid therapy based on subjective and objective assessments? STUDY DESIGN AND METHODS: A prospective cohort of patients with fibrotic HP diagnosed per American Thoracic Society/Japanese Respiratory Society/Asociación Latinoamericana del Tórax guidelines was recruited. Baseline assessments included cough visual analog scale (VAS) and Leicester Cough Questionnaire (LCQ) score. Cough frequency was assessed using the VitaloJAK (Vitalograph) cough monitor in a subset of patients. Multivariable models evaluated predictors of cough severity, and in incident cases, changes in cough outcomes were evaluated after 3 months of corticosteroid therapy. RESULTS: A total of 101 patients were recruited (41 male patients; mean age, 65 years). The median cough VAS was 35 mm (interquartile range [IQR], 14-50 mm) and the median LCQ score was 15.2 (IQR, 13.2-17.4). The median cough count was 8.7/h (range, 0.2-32.1/h; n = 28). Subjective cough scores correlated with objective cough frequency (cough VAS, ρ = 0.69 [P < .001] and LCQ score, ρ = -0.555 [P = .002]). Female sex, reduced FVC, and higher bronchoalveloar lavage lymphocyte fractions were independent predictors of worse cough severity, as measured by cough VAS. Corticosteroids significantly improved cough subjectively (cough VAS, -13.7 mm [P = .002] and LCQ score, +1.9 [P < .001]; n = 44), but did not significantly reduce objective cough frequency (n = 16). Lung function remained unchanged at 3 months. INTERPRETATION: Our results show that cough is a major symptom for patients with HP. Although corticosteroids
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Journal articleJenkins G, 2026,
A statistical model for lung function trajectory and mortality in patients with fibrotic interstitial lung disease
, American Journal of Respiratory and Critical Care Medicine, ISSN: 1073-449XBackground. Fibrotic interstitial lung diseases (ILDs) cause loss of forced vital capacity (FVC) and increased risk of death over time. Most clinical trials aim to slow FVC decline and reduce mortality. However, the association of lower FVC with higher mortality will bias simple estimates of differences in FVC progression between groups. Therefore, both the time-dependent decline in FVC and increase in mortality should be jointly modelled.Methods. We developed a Bayesian, joint mixed effects disease progression model (DPM), using minimally informative prior distributions, for FVC trajectory and the hazard for ILD-related mortality over time. This model minimizes bias due to mortality in estimating differences in the rate of FVC decline and is suitable for use when characterizing populations or in estimating a treatment effect in a clinical trial. The DPM was applied to individual patient data from prospective cohort studies of fibrotic ILD.Results. The DPM yields a higher estimated rate of FVC decline (6.0 vs 4.7%/year) and a more precise fit than a linear mixed model of FVC alone, and replicates the non-linear pattern in the observed data. By modelling the full FVC trajectory rather than only the change from baseline at a given time point, the DPM increases the information from each patient and reduces both the time to information and the effect of variability in baseline FVC measurements on the estimation of treatment effects.Conclusions. The joint DPM provides an integrated approach to minimizing bias in the estimation of treatment effects in clinical trials in fibrotic ILDs.
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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, Vol: 25, ISSN: 1474-9718Ageing 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 articleBonner KL, Fontanella S, Gore M, et al., 2026,
Lower airway immunophenotyping in severe preschool wheeze reveals distinct clusters described by heterogeneity in neutrophil phenotypes.
, Am J Respir Crit Care Med, Vol: 212, Pages: 733-745RATIONALE: Recurrent preschool wheeze accounts for most childhood hospitalizations for asthma and often responds poorly to inhaled corticosteroids (ICSs). OBJECTIVE: To relate lower airway immune cell composition in children with recurrent severe wheeze (RSW) to infection, allergic sensitization, and prescribed treatments. METHODS: Children with RSW aged 1 to 5 years underwent clinical phenotyping, bronchoscopy, multiparameter flow cytometry of blood and bronchoalveolar lavage (BAL) to characterize leukocytes, and assessments of lower airway bacterial and viral infection. An unsupervised analysis was undertaken to uncover clusters of airway inflammation. MEASUREMENTS AND MAIN RESULTS: Of 106 children (median age 36.5 months), 32% had allergic sensitization. Lower airway immune cells were similar in type and abundance in sensitized and nonsensitized children. However, significantly more nonsensitized wheezers had positive BAL bacterial culture. Bacterial infection was associated with neutrophils with low CD62L and CXCR2 expression. Children without airway bacterial infection also had up to 50% neutrophils but with high CD62L and CXCR2 expression. The data-driven analysis revealed 3 clusters: cluster 1, airway infection predominant with CD62Llo neutrophils; cluster 2, eosinophil/lymphocyte rich with CD62Lhi neutrophils; and cluster 3, low infection rate with CD62Lhi neutrophils. The clusters were independent of clinical features, prescribed ICSs, antibiotics, and allergic sensitization. CONCLUSIONS: Airway inflammation in RSW is heterogeneous. A subgroup had airway neutrophilia but with distinct neutrophil subtypes. Those with bacterial infection had CD62Llo neutrophils (cluster 1). Others had CD62Lhi neutrophils (clusters 2 and 3). Intervention trials stratifying using these clusters may provide a novel management approach.
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Journal articlePhilip K, Feifei B, Buttery S, et al., 2026,
The relationship of breathlessness with social isolation and loneliness: a nationally representative cohort study of older adults in England
, BMJ Public Health, Vol: 4, ISSN: 2753-4294Introduction Breathlessness is a common and distressing symptom impacting quality of life and limiting activities of daily living. Social isolation and loneliness are associated with increased morbidity and mortality, being problems in themselves and risk factors for poor health. Qualitive studies indicate breathlessness impacts social health, however quantitative evaluation is limited. We aimed to assess the relationship of breathlessness with social isolation and loneliness in adults. Methods Using a nationally representative sample of older adults aged ≥50years from the English Longitudinal Study of Ageing (N=6,623). The sample had 44% males, mean age of 70years (SD=10). We examined associations of baseline breathlessness (mMRC breathlessness scale) with loneliness (3-item UCLA loneliness scale) and social isolation (low social contact, low community participation, living alone), at baseline, and follow-up at 4- and 8-years later, using regression models adjusted for confounders. Results At baseline, breathlessness was associated with higher levels of loneliness (coef.=0.161, 95%CI 0.1130.209), and social isolation, including low social contact (coef.=0.094, 95%CI 0.028-0.159), low community participation (coef.=0.169, 95%CI 0.117-0.221), and living alone (OR 1.089, 95%CI 1.0261.157). Longitudinally, breathlessness was associated increasing loneliness and reducing social contact and community participation at 4 and 8-year follow-up. Breathlessness was not associated with change in living alone. Findings were independent of identified confounders. Conclusions Breathlessness is related to increasing social isolation and loneliness, potentially due to limiting the amount and quality of social interactions. These findings suggest important psychosocial impacts of breathlessness requiring holistic management strategies.
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