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Journal articleWen H, Kole T, Carpaij OA, et al., 2026,
Nasal Airway Transcriptome Reflects Selected Asthma-Associated Gene Signatures in the Lower Airways.
, Allergy, Vol: 81, Pages: 3197-3205BACKGROUND: 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 articleVieira RJ, di Bona D, Bognanni A, et al., 2026,
Estimating Work-Related Indirect Costs in Allergic Rhinitis and Asthma Using a Daily Combined Symptom-Medication Score: A MASK-air Study in Collaboration With the EAACI Methodology Committee.
, J Allergy Clin Immunol Pract, Vol: 14, Pages: 2143-2154.e6BACKGROUND: Allergic rhinitis and asthma can impair work productivity. OBJECTIVE: To validate a daily work productivity visual analogue scale (VAS work), comparing it with the Work Productivity and Activity Impairment questionnaire plus Classroom Impairment Questions: Allergy Specific (WPAI+CIQ:AS) and also to quantify how allergy control relates to work impairment and indirect costs. METHODS: We conducted a cross-sectional study using data from the MASK-air app. Patients recorded daily VAS and weekly WPAI+CIQ:AS responses. We calculated correlations between VAS work and WPAI+CIQ:AS outcomes. Mixed-effects regression models assessed associations between disease control, measured by the Combined Symptom-Medication Score (CSMS) and the electronic daily asthma control score (e-DASTHMA), and VAS work. Indirect costs were estimated using the human capital approach, applying VAS-based productivity losses to country-specific wage distributions. RESULTS: VAS work correlated strongly with the WPAI+CIQ:AS, with Spearman coefficients 0.70 or higher for total work impairment and presenteeism. Each 1-point increase in CSMS and e-DASTHMA was associated with mean 0.97- and 0.79-point increases in VAS work, respectively. On poorly controlled days, the estimated daily indirect cost based on CSMS ranged from US $12.50 purchasing power parities (PPP) (P25-P75, 5.60-26.70) in Brazil to US $129.90 PPP (P25-P75, 80.40-199.40) in Iceland. Based on e-DASTHMA, daily estimates ranged from US $9.30 PPP (P25-P75, 3.70-21.50) in Brazil to US $101.90 PPP (P25-P75, 51.20-172.40) in Iceland. CONCLUSIONS: VAS work is a valid simple daily measure of work impairment due to rhinitis and asthma. CSMS and e-DASTHMA can be used to estimate productivity losses attributable to poor disease control.
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Journal articleSaunders LC, Collier GJ, Smith LJ, et al., 2026,
Longitudinal 1H and 129Xe Lung MRI in Patients With Post-COVID Residual Lung Abnormalities.
, J Magn Reson Imaging, Vol: 64, Pages: 669-682BACKGROUND: It is unclear how lung function may recover in patients with residual lung abnormalities (RLAs) following COVID-19 pneumonia. PURPOSE: To evaluate lung function trends over time in patients with RLAs following hospitalization due to COVID-19. STUDY TYPE: Prospective, multicenter longitudinal cohort study. POPULATION: Twenty-four participants hospitalized due to COVID-19 with RLAs identified on CT ≥ 3 months postdischarge (median [IQR] age 69 (15) years; 3 female) underwent at least one MRI at 6 months (n = 16), 1 year (n = 19), or 2 years (n = 14). FIELD STRENGTH/SEQUENCE: 1.5 T. Dynamic contrast enhanced (DCE) 3D spoiled gradient echo, 129Xe steady state free precession (ventilation), 129Xe 3D spoiled gradient echo multiple b-value (diffusion-weighted), 129Xe 4-echo flyback 3D radial (dissolved phase). ASSESSMENT: Pulmonary blood flow, volume, and mean transit time (MTT) were calculated from DCE MRI. The fraction of 129Xe signal in the red blood cells to membrane (RBC:M) was calculated from the dissolved phase 129Xe acquisition. Ventilation defect percentage (VDP) was calculated from the 129Xe ventilation acquisition. Mean diffusive length scale (LmD) was calculated from the 129Xe diffusion-weighted acquisition. STATISTICAL TESTS: Changes in metrics with time and associations between metrics were assessed using mixed-effect linear regression. Correlations were tested using Spearman's correlation coefficient. Regional differences were assessed using a Friedman's test with a Bonferroni adjustment. p < 0.05 was considered significant. RESULTS: Pulmonary blood flow and MTT improved significantly over time (MTT: 6 months, 15.3 (IQR, 2.0); 1 year, 15.6 (1.4); 2 years, 15.0 (5.3); pulmonary blood flow: 6 months, 75.4 (IQR, 22.0); 1 year, 83.2 (47.4); 2 years, 107.3 (51.1)). RBC:M z-score was low at all three visits (
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Journal articlePortacci A, Ventura L, Menzella F, et al., 2026,
Small airway dysfunction may mediate the association between body mass index and severe asthma exacerbations.
, Eur Respir J, Vol: 68BACKGROUND: Obesity is associated with poorer asthma outcomes and an increased risk of exacerbations, but the underlying mechanisms remain incompletely understood. Small airway dysfunction (SAD) may represent a key mechanistic link between excess body weight and adverse asthma outcomes. METHODS: In this multicentre observational study, adult patients with asthma underwent clinical characterisation, spirometry and impulse oscillometry (IOS). SAD was defined using a composite criterion based on small airway resistance (frequency dependence of resistance between 5 and 20 Hz (R 5-20)), reactance area (AX) and ratio of peripheral airway to total airway resistance ((R 5-20)/R 5). Associations between body mass index (BMI), SAD and severe asthma exacerbations were assessed using multivariable regression models. Non-linear relationships were explored using generalised additive models, and mediation analyses quantified the contribution of SAD to the obesity-exacerbation association. RESULTS: Among 1169 patients, IOS-defined SAD was significantly more prevalent in individuals with BMI ≥30 kg·m-2. Increasing BMI was associated with worse IOS parameters (p<0.0001), following a non-linear pattern with steeper deterioration beyond BMI values of ∼28-30 kg·m-2. SAD was independently associated with obesity (adjusted OR 2.11, 95% CI 1.56-2.86) and with severe asthma exacerbations in the previous year (adjusted OR 2.01, 95% CI 1.53-2.65) (both p<0.0001). Mediation analyses showed that SAD accounted for 26-41% of the association between obesity and exacerbation risk (p=0.004 and p=0.03). Spirometry indices provided limited additional information. CONCLUSION: Oscillometry-defined SAD represents a non-linear functional trait underlying the association between obesity and severe asthma exacerbations, supporting its clinical relevance in obese patients with asthma and identifying SAD as a potential treatable trait.
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Journal articleWang H, Fung NH, Aloe C, et al., 2026,
CCR2/CCR5 Signaling Defines a Pathogenic Interstitial Macrophage Subset That Drives Severe Asthma.
, Clin Transl Allergy, Vol: 16, ISSN: 2045-7022BACKGROUND: Severe asthma is a chronic inflammatory disease characterised by airway dysfunction, persistent immune activation and corticosteroid resistance. While macrophages are key regulators of lung immunity, how individual subsets, particularly interstitial macrophages (IMs), contribute to disease remains poorly understood. METHODS: Lung macrophages were profiled using single-cell RNA-sequencing (scRNA-seq) and flow cytometry in a C57BL/6 mouse model of severe asthma induced by Complete Freund's Adjuvant (CFA) and house dust mite (HDM). Human transcriptomic data from the U-BIOPRED asthma cohort were analyzed for translational validation. The dual CCR2/CCR5 antagonist Cenicriviroc (CVC) was used to evaluate the therapeutic potential of targeting pathogenic macrophages. RESULTS: CFA-HDM treatment led to marked depletion of resident alveolar macrophages (rAMs) and their replacement by recruited AMs (recAMs) associated with tissue remodeling. A distinct Lyve1loMHCIIhi IM subset emerged as the dominant inflammatory cell population, displaying high Ccr2 and Ccr5 expression, potent pro-inflammatory and antigen-presenting signatures, and extensive ligand-receptor communication with T cells, neutrophils and rAMs. Trajectory analysis demonstrated that both recAMs and Lyve1loMHCIIhi IMs arise from classical monocytes. Consistently, sputum transcriptomic data from the U-BIOPRED asthma cohort showed reduced AM-associated gene signatures and enrichment of IM/monocyte and CCR-chemokine programs in patients with severe disease. Pharmacological blockade of CCR2/CCR5 with CVC markedly reduced IM infiltration, limited T-cell and neutrophil recruitment, restored macrophage balance, and improved lung function. CONCLUSIONS: Lyve1loMHCIIhi IMs orchestrate airway inflammation in severe asthma. Dual CCR2/CCR5 antagonism inhibits their recruitment, restores macrophage balance, and halts disease progression, highlighting this pathway as a promising therapeutic target.
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Journal articleDhochak N, Robinson PFM, Saglani S, 2026,
Update on Pediatric asthma management: Recent advances.
, Pediatr Allergy Immunol, Vol: 37Asthma remains the commonest chronic pediatric respiratory disease and a major cause of childhood morbidity worldwide. Recent advances in pediatric asthma management shift the focus from symptom relief alone towards early control of airway inflammation, exacerbation prevention, and personalizing biomarkers to target biologics. This review highlights the growing role of anti-inflammatory reliever [AIR] therapy and maintenance-and-reliever therapy [MART], both of which incorporate inhaled corticosteroids [ICS] with bronchodilator treatment to reduce reliance on short-acting β2-agonists [SABA]. Pediatric clinical trials demonstrate that strategies including AIR only and MART, compared to SABA reliever, reduce acute asthma attack burden in some disease subgroups while further large trials are underway. For severe pediatric asthma, advances in understanding type 2 airway inflammation have led to the introduction of biologics targeting key inflammatory pathways, including IgE, interleukin (IL)-5, IL-5 receptor, IL-4/IL-13 signaling, and thymic stromal lymphopoietin. Adult trials have shown reductions in asthma attacks with all currently licensed biologics. Although pediatric evidence remains more limited than in adults, we summarize the current evidence of efficacy in childhood severe asthma. Biomarker-guided selection using blood eosinophils, fractional exhaled nitric oxide, and serum IgE is increasingly important, yet optimal pediatric biomarkers of response remain uncertain. Current challenges include gaps in child-specific biomarker validation and uncertainty regarding treatment duration and discontinuation strategies. Overall, contemporary pediatric asthma management is moving towards precision medicine, integrating anti-inflammatory reliever strategies and targeted biologics to improve disease control, minimize exacerbations, and preserve long-term lung health.
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Journal articleRoth-Walter F, Adcock IM, Benito-Villalvilla C, et al., 2026,
Update on Non-Biological and RNA-Based Therapeutics in Chronic Inflammatory Diseases: Precision Medicine Through Small Molecules: An EAACI Position Paper.
, Allergy, Vol: 81, Pages: 3039-3070In the last decades, critical advancements in research technology and knowledge on disease mechanisms steered therapeutic approaches for chronic inflammatory diseases towards unprecedented target specificity. For allergic and chronic lung diseases, biologic drugs pioneered this goal, acquiring on the way-through the clinical use of monoclonal antibodies-a deeper understanding of how inflammatory and immune pathways are configured in disease-specific patterns. In this biomarker-driven approach, synthetic small molecule drugs (SMDs) were perceived as lagging behind in innovation for their relative lack of specificity. This was, however, mostly due to a shift in focus towards biologics rather than true obsolescence of SMDs. In the same timeframe, in fact, advances in structural biology and medicinal chemistry, bioinformatics and artificial intelligence held steadily SMDs' innovation and relevance. The use of kinase inhibitors, well established in the treatment of cancer and rheumatological diseases, is now approved for some allergic skin diseases and is approaching asthma and COPD with several clinical trials; moreover, new therapeutics targeting mast cell receptors and molecules involved in innate immunity are entering preclinical and clinical testing. Alongside, the portfolio of biologics is harboring the expansion of RNA therapeutics, which gained global recognition during the COVID-19 pandemic due to RNA vaccines. Different types of RNA therapeutics, including those based on different non-coding RNAs, are advancing to agency approval and market, thanks to improvements in molecule stability and delivery systems. In summary, the evidence presented in this position paper illustrates that precision medicine is becoming a goal shared between synthetic SMDs and biologics, both protein/antibody-based and RNA therapeutics. We review the current state, unmet needs and opportunities within this evolving landscape, highlighting how small molecular species, both synthetic as S
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Journal articleTran XN, Lee Y-L, Chang L-T, et al., 2026,
Climate change, environmental exposures, and pediatric asthma exacerbations: air pollution, temperature, and relative humidity.
, Pediatr ResThe prevalence of pediatric asthma exacerbations (AEs) has risen alongside climate change, yet how climate change modifies these exposures to raise pediatric AEs remains unclear. This review synthesizes epidemiological and mechanistic evidence on the contribution of air pollution, temperature, and relative humidity (RH) to pediatric AEs under climate change, drawing on a narrative search of PubMed and Web of Science (2000-2025) prioritizing systematic reviews, epidemiological studies, and climate-attribution/modeling studies. Climate change intensifies environmental drivers of AEs, to which children's higher ventilation and reactive airways heighten susceptibility. Air pollutants trigger oxidative stress, epithelial injury, and type 2 inflammation, while rising temperatures and extreme weather increase oxidative stress, C-fiber activation, and systemic inflammation. Climate-driven shifts in RH cause airway dehydration at low humidity and impaired mucus clearance at high humidity. Lengthening pollen seasons, transitional-weather viral circulation, and more frequent wildfires, hurricanes, floods, and dust storms further increase exacerbation risk. Climate-driven environmental changes contribute to pediatric AEs, though attribution is quantified for only selected exposures. Prevention strategies, including heat- and air-quality warning systems, environmental adaptation, and equity-focused targeting of high-risk populations, are needed. IMPACT: Climate change amplifies environmental triggers of pediatric asthma exacerbations, a burden concentrated among disadvantaged children by socioeconomic and structural disparities. Children's physiological vulnerability heightens their sensitivity to these triggers. Closing pediatric-specific attribution gaps and integrating climate-adaptation strategies into asthma care could reduce this burden.
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Journal articleTorres MJ, Atanaskovic Marković M, Gelincik A, et al., 2026,
EAACI Spring Meeting 2026: Prevention as Treatment-A New Paradigm.
, Allergy -
Journal articleKc S, Hopkinson NS, Neves AL, et al., 2026,
Impact of Patient Portals on Asthma and Chronic Obstructive Pulmonary Disease-Related Quality-of-Care Outcomes: Systematic Review.
, Online J Public Health Inform, Vol: 18, ISSN: 1947-2579BACKGROUND: Patient portals are increasingly used to support self-management and facilitate care coordination in people with chronic diseases. Although some asthma quality-of-care gains and modest chronic obstructive pulmonary disease (COPD) improvements have been reported in wider digital health studies, a comprehensive review of patient portal-specific evidence is lacking. OBJECTIVE: This study aimed to systematically synthesize evidence on the impacts of patient portals on adult asthma and COPD outcomes across 6 quality-of-care domains (effectiveness, patient-centeredness, equity, efficiency, safety, and timeliness). METHODS: We searched 5 databases (MEDLINE/PubMed, Embase, PsycINFO, CINAHL, and Google Scholar) for quantitative evaluations published up to March 2026 (CRD42022316044). The Newcastle-Ottawa Scale and Cochrane Risk of Bias-2 tool were used for quality assessments, and certainty of evidence was evaluated using the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) approach. Findings were narratively synthesized using the SWiM (Synthesis Without Meta-analysis) framework. RESULTS: We identified 4038 records, and 16 papers published between 2007 and 2024 met the inclusion criteria (asthma=13, COPD=2, both=1). Three were randomized controlled trials, all rated high risk of bias. Of the other studies, 5 had low risk, 6 had moderate risk, and 2 had high risk of bias. Effectiveness and patient-centeredness were most frequently reported, with 12 papers each. Eight papers were on equity, 5 each on efficiency and safety, and 4 on timeliness. In asthma, modest disease control improvements were reported in 27.8% (42/151) of participants using patient portals with home visit support versus portal use alone (35/150, 23.3%). In COPD, one large, interrupted time series study (N=909,724) reported post-implementation reductions in hospitalizations (slope change from 1.33 to -4.38 per 10,000 patients per month; P<.001) but no mortality benefit
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Journal articleWang R, Chen Y, Liu X, et al., 2026,
Extracellular vesicles in senescence-associated chronic lung diseases.
, Chin Med J (Engl), Vol: 139, Pages: 2392-2408Chronic lung diseases, such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, obstructive sleep apnea, asthma, bronchiectasis, and lung cancer, are intricately linked to the aging process. These diseases are characterized by a high prevalence rate and a paucity of effective treatment options. Emerging evidence highlights the critical role of extracellular vesicles (EVs) in the pathogenesis and progression of these diseases. EVs, released by senescent cells, mediate intercellular communication and modulate immune responses through their cargo of microRNAs, proteins, and other molecules. These vesicles contribute to disease progression by promoting inflammation, fibrosis, tissue remodeling, and cellular senescence. Specifically, certain microRNAs, such as miR-21, miR-34a, and miR-570-3p, along with several proteins in EVs, have been identified as key factors influencing these processes. Additionally, EVs play significant roles in immune regulation and have potential anti-inflammatory effects, making them promising candidates for therapeutic applications. Recent advances in the use of EVs as therapeutic agents, including their application in nanotechnology for targeted drug delivery, have demonstrated potential in reducing inflammation, modulating immune responses, and enhancing tissue repair. Understanding the role of EVs in these diseases offers insights into potential therapeutic targets to mitigate disease progression and improve patient outcomes. Future research should focus on standardizing EV isolation and characterization methods, verifying the safety and efficacy of EV-based therapies in clinical trials, and elucidating the complex biological mechanisms of EVs in aging and disease.
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Journal articleHillson K, Oritz KM, Hay S, et al., 2026,
High oral corticosteroid use during acute attacks of preschool wheeze irrespective of clinical phenotype
, Archives of Disease in Childhood, ISSN: 0003-9888Objective This study aims to evaluate the burden of oral corticosteroid (OCS) use and any relationship to clinical phenotype in preschool children presenting with acute wheeze attacks.Methods Single-centre prospective study in which children with recurrent, severe preschool wheeze (PSW), who were referred to a tertiary respiratory centre, had symptom questionnaire, point-of-care blood eosinophil count (BEC) and aeroallergen sensitisation tests undertaken on the same day as their outpatient clinic appointment.Results 100 children with PSW (median age 3.5 years; IQR 2.8–4.9 years; 51% male) were recruited. Clinical atopy, based on parental reporting, was present in 42%, while objective sensitisation, confirmed by testing, was observed in 35%. Median lifetime OCS courses per child was 10 (IQR 6–18) and 5 (IQR 3–7) during the preceding 12 months. Regardless of which definition of atopy was used, atopic children had higher BEC when well, compared with non-atopic children: using clinical atopy classification, median BEC was 0.65 versus 0.3×10⁹/L (p=0.003) and using objective atopy, median BEC was 0.7 versus 0.3×10⁹/L (p<0.0001). There was no difference in the use of OCS in the acute setting between higher and lower BEC, between clinical or objective atopy or a combination of these either over the child’s lifetime or during the previous 12 months.Conclusion Children with severe, recurrent PSW are being treated with large numbers of OCS courses despite the lack of evidence of significant efficacy. There is an urgent need for trials which include phenotyping of acute attacks to guide OCS treatment.
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Journal articleGerth van Wijk R, Mahler V, Albrecht M, et al., 2026,
Factors for Success and Failure of Allergen Immunotherapy (AIT) Trial Design in the Light of Evidence-Based Medicine: Current Aspects 2026.
, AllergyAllergen immunotherapy (AIT) has been acknowledged as the only disease-modifying treatment for respiratory diseases since its introduction in 1911. Although the efficacy and safety have convincingly been established in numerous randomized clinical trials (RCTs), the AIT study results may vary substantially. Several factors that may influence the outcome of RCTs will be addressed. First, the choice of the primary endpoint is essential. Lack of validated endpoints with proven clinical relevance may contribute to the variation in study results. Secondly, heterogeneity of the patient population affects the study outcome, thereby raising the question of whether current selection criteria should be further optimized to capture those patients who will benefit from immunotherapy. Thirdly, variability and particularly low allergen exposure may lead to unsuccessful AIT trials. Fourthly, unsuccessful trials may stem from large placebo effects. Furthermore, discrepancies between Phase II and III studies are asking for cautious interpretation of Phase II studies when planning Phase III studies. Flaws in trial design, inadequate reporting of the clinical trial protocol and data may hamper the interpretation of study results. In addition, this review addresses specific aspects of AIT trial design in children and asthmatic patients. To improve future AIT trials, innovative solutions are urgently needed, including the establishment of an internationally accepted minimal clinically important difference (MCID), the validation of primary endpoints, the integration of field studies and allergen exposure chamber studies, and the publication of negative study results.
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Journal articleCanizales J, Schofield S, Shamji MH, et al., 2026,
Patterns of mouse allergen–specific IgE and IgG4 in contemporary animal research environments
, Clinical and Experimental Allergy, Vol: 56, Pages: 983-985, ISSN: 0954-7894 -
Journal articleWu Z, Moor K, Wijsenbeek MS, et al., 2026,
The Impact of Disease Severity and Symptoms on Anxiety and Depression in Individuals With Idiopathic Pulmonary Fibrosis.
, Chest, Vol: 170, Pages: 467-476BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a debilitating, life-limiting fibrotic lung disease. Symptoms including breathlessness, cough, and fatigue, together with disease severity, contribute to psychological burden, yet their relationship with anxiety and depression remains unclear. RESEARCH QUESTION: In patients with IPF, what is the prevalence and severity of anxiety and depression, and what are their associations with symptoms and disease severity? STUDY DESIGN AND METHODS: This observational study prospectively recruited patients with incident IPF. Hospital Anxiety and Depression Scale (HADS), Dyspnea-12, Leicester Cough Questionnaires, cough visual analog scales, Living with IPF (L-IPF), and lung function were assessed at baseline and 12 months. RESULTS: Two hundred sixty-nine patients with IPF (mean age, 73.5 years; 81% male) were recruited; 157 completed follow-up. Mean FVC % predicted ± SD was 79% ± 14.7%. At baseline, the prevalence of anxiety and depression (HADS score ≥ 8) was 27.5% and 28.3%, respectively (suggestive HADS 8-10: 18.6% and 14.9%; probable HADS ≥ 11: 8.9% and 13.3%, respectively). On multivariable analysis, worse Dyspnea-12 and poorer L-IPF energy were independent factors for both anxiety and depression at baseline; younger age was a factor for anxiety. Baseline lung function did not correlate with HADS anxiety or HADS depression. At follow-up, HADS anxiety scores increased numerically, below reported minimal clinically important difference values, with no change in HADS depression scores. Younger age, higher Dyspnea-12 scores, and poorer L-IPF energy were associated with greater increases in anxiety. Moderate or weak correlations were observed between changes in HADS and longitudinal changes in patient-reported outcomes (worsening breathlessness, cough, and energy levels). Changes in FVC % predicted did not correlate with HADS. INTERPRETATION: Our results show that anxiety and depression are common in patient
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Journal articlePeter J, Jindal A, Del Giacco S, et al., 2026,
Urticaria and Angioedema: When East Meets West-and the Middle.
, Allergy, Vol: 81, Pages: 2579-2581 -
Journal articleChae W, An J, Lee W, et al., 2026,
Circulating 1-Methylnicotinamide Predicts Dupilumab Response in Adult Asthma: A Prediction Model.
, Clin Exp Allergy, Vol: 56, Pages: 935-938Plasma 1‐methylnicotinamide is elevated in dupilumab responders, outperforming conventional type‐2 biomarkers. Combining 1‐methylnicotinamide with FeNO achieves the highest predictive accuracy for dupilumab treatment response.
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Journal articleWilson-Morkeh H, Seluk L, Bosch P, et al., 2026,
Targeting Immunologic Pathways in Eosinophilic Granulomatosis With Polyangiitis: Translating Emerging Evidence Into Clinical Practice.
, Allergy, Vol: 81, Pages: 2775-2791Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare and potentially life-threatening systemic, inflammatory disease with multi-organ manifestations, variable presentation and complex pathology. Multiple interconnected immunological pathways are implicated in EGPA pathology, including a type-2 immune response driving predominantly eosinophilic inflammation, B-cell mediated autoimmunity, neutrophil activation, and the generation of pathogenic anti-neutrophil cytoplasmic antibodies, all of which can contribute to tissue/organ damage. High-dose glucocorticoids are the mainstay treatment for EGPA, but over the past two decades the development of biologic treatments targeting interleukin (IL)-5, eosinophils and B-cells has revitalized the treatment landscape. Mepolizumab, a humanized monoclonal antibody that specifically targets IL-5, and benralizumab, which targets the IL-5 receptor (IL-5Rα), are both approved for the treatment of patients with non-severe relapsing or refractory EGPA. In Phase III trials, these biologics have demonstrated favorable safety profiles and efficacy, with treatment leading to remission induction, remission maintenance, and oral glucocorticoid sparing benefits. However, as understanding of the full complexity of EGPA pathogenesis improves, new treatment targets are emerging. Consequently, understanding key pathogenic mechanisms at the patient level, enabling a more tailored treatment approach, is an important goal for future research.
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Journal articleBaylis S, Hopkinson NS, Feliu A, et al., 2026,
Statement of the European Respiratory Society on the tobacco endgame.
, Eur Respir J, Vol: 68 -
Journal articleKuks PJM, Aabed AMA, Premereur LCA, et al., 2026,
Clinical phenotyping of asthma patients with elevated sputum eosinophils and low blood eosinophils: a post-hoc analysis of the multicentre ATLANTIS cohort.
, EBioMedicine, Vol: 130BACKGROUND: Patients with eosinophilic asthma are responsive to treatment with corticosteroids and biologics. Eosinophilia is usually identified based on blood eosinophil counts, but there is discordance between blood and sputum in some cases. A subset of patients may have sputum eosinophilia despite low blood eosinophil levels. The clinical implications of this so-called isolated sputum eosinophilia are unknown. The aim of this study is to investigate the clinical expression of asthma in patients with isolated sputum eosinophilia. METHODS: In this post-hoc ATLANTIS analysis we included patients with available blood and/or sputum data from ATLANTIS. Patients were classified according to blood eosinophils (< or ≥300 cells/μL). Patients with isolated sputum eosinophilia were compared with those with low eosinophils in both compartments. FINDINGS: Of the 487 patients with low blood eosinophils counts, sputum samples were available in 146. Among these, 25 (17%) had isolated sputum eosinophilia. Compared with patients with low eosinophils in both compartments (n = 121), patients with isolated sputum eosinophilia had more airflow obstruction (FEV1/FVC ratios (68.8% vs. 75.4%, p <0.01)) and small airways dysfunction (Scond0.05 vs. 0.03 1/L, p = 0.02) and more frequently reported exacerbations in the year prior to inclusion (28% vs. 9%, p = 0.01). Clinical characteristics were broadly comparable to those observed in patients with blood eosinophilia. INTERPRETATION: Isolated sputum eosinophilia occurs in a subgroup of patients with asthma, in association with worse clinical outcomes. These findings suggest that airway eosinophilia may not always be captured by conventional blood biomarkers and warrant further investigation into the clinical implications of this phenotype to determine whether these patients may benefit from treatment strategies targeting type 2 inflammation, such as intensified steroids or biologics. FUNDING: Chiesi Farmaceutici sponsored the ATLA
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