Dear Editor,The article “Nurse-Led Family Interactive Intervention in Children with Bronchopneumonia: A Randomized Controlled Trial” by Fang Wu (2026) explores the influence of a nurse-led family i...

Objective To provide a clinically grounded and pathobiological review of eosinophilic inflammation in severe asthma, addressing mechanisms, diagnostic interpretation, and implications for biologic therapy selection. Methods Narrative review of guidelines, pivotal phase 2–3 randomized controlled trials, meta-analyses, registry data, and key translational studies evaluating eosinophils, type 2 (T2) inflammation, and targeted biologic therapies in severe asthma and eosinophilic chronic obstructive pulmonary disease. Publications were selected based on clinical relevance, methodological rigor, and impact on contemporary severe asthma management. Evidence was critically appraised and integrated with expert clinical perspective. No predefined systematic protocol or formal risk-of-bias assessment was undertaken. Results Eosinophils are central effector cells in T2-high severe asthma, contributing to airway inflammation, epithelial injury, mucus plugging, and remodeling. Interleukin (IL)-5 is the principal regulator of eosinophil maturation and survival, while IL-4, IL-13, and epithelial alarmins modulate tissue recruitment and amplification of inflammation. Blood eosinophil count (BEC) remains the most accessible biomarker in practice; however, its interpretation requires contextualization, considering corticosteroid exposure, biological variability, age at onset, and comorbidities. No single biomarker fully reflects airway eosinophilia, supporting a multidimensional assessment integrating clinical phenotype, longitudinal biomarkers, imaging, lung function, and therapeutic response. Biologics have transformed outcomes, with greater efficacy generally observed at higher BEC levels. Conclusion Eosinophilia should be interpreted as a contextual biomarker within a comprehensive clinical framework. Precision phenotyping is essential to optimize biologic selection and advance toward sustained disease control and clinical remission in severe asthma.

ABSTRACT Objective To assess whether a World Asthma Day campaign could provide epidemiological information, identify possible undiagnosed asthma, and increase public awareness of the disease. Methods On World Asthma Day 2024, an information desk staffed by pulmonology, allergy, and nursing professionals was installed in the hospital lobby, and volunteers were invited to participate. Recorded variables included age, sex, body mass index, smoking status, previous asthma diagnosis, rhinitis, asthma severity, medical follow-up, previous spirometry, asthma treatment, and comorbidities. Respiratory symptoms compatible with asthma were assessed using a brief structured mini-questionnaire enquiring about recurrent wheezing, persistent or recurrent cough, exertional dyspnoea, nocturnal symptoms, and chest tightness. Spirometry and fractional exhaled nitric oxide were measured in all participants. Asthma control was assessed using the Asthma Control Test. Results A total of 112 volunteers were evaluated (mean age 57 ± 18 years; 84 women, 75%). Known asthma was present in 45 participants (40%), rhinitis in 46 (41%), and comorbidities in 51 (46%). Among participants with known asthma, 42.2% reported no active follow-up, and 46.7% were not on maintenance therapy. Fourteen participants (12.5%) fulfilled criteria for probable undiagnosed asthma (compatible symptoms plus fractional exhaled nitric oxide ≥25 ppb). The campaign reached 12,500 social media users with an engagement rate of 18.4%. Conclusions This campaign was useful not only for identifying potential new asthma cases, but also for increasing disease awareness through substantial media and social-media impact.

To the editor,We thank Miao et al. for their interest in the FORCE2 study [1], and for the opportunity to clarify aspects of the run‑in design and its implications for the trial’s primary endpoint ...

Background Pentraxin-3 (PTX-3) is a humoral pattern recognition receptor involved in innate immunity and inflammation regulation, but its relationship with lung function remains unclear. Objective This study investigated the association between serum PTX-3 levels and respiratory function in preschool wheezy children (CW), considering wheezing phenotypes and atopy. Methods In this cohort study, 165 preschoolers were divided into 84 wheezy children (CW) and 81 healthy controls (HC). Serum PTX-3 levels, eosinophil counts, and pulmonary function using impulse oscillometry (IOS) were assessed. IOS parameters included zR5, zR20, R5-20, zX5, zX20, Fres, and AX. Comparisons were made according to wheezing phenotype (multi-trigger vs episodic) and atopy status. Correlation analysis between PTX-3 and IOS parameters was performed. Results The CW group had higher PTX-3 levels (p = 0.010), increased IOS parameters (zR5, zR20, R5-20, Fres, AX; p < 0.05), and reduced zX5 (p < 0.001). PTX-3 positively correlated with zR5, zR20, and AX (r:0.220–0.226, p < 0.05). Multi-trigger wheezing and atopy were associated with higher R5-20 and PTX-3 (p < 0.05). Children with parental atopy also showed higher PTX-3 and airway resistance. Conclusion Elevated PTX-3 is associated with impaired lung function in preschool wheezy children and may serve as a biomarker for respiratory function, phenotype differentiation, and atopy.

Objectives a key feature of asthma is airway hyperresponsiveness (AHR), which is typically diagnosed through methacholine challenge testing (MCT). Fractional exhaled nitric oxide (FENO) is a noninvasive marker of type-2 inflammation. Extended nitric oxide analysis breaks this down into bronchial (JawNO) and alveolar (CANO) components; we aimed to determine whether this extensive analysis offers added value in diagnosing AHR beyond what conventional FENO testing can provide. Methods seventy-two consecutive patients referred for MCT were prospectively enrolled and underwent spirometry, extended nitric oxide analysis, and MCT. AHR was defined using three methacholine dose thresholds for PD20FEV1 (≤400, ≤800, and ≤1600 µg). Results AHR prevalence ranged from 23.6% at the lowest threshold (≤400 µg) to 44.4% at the highest (≤1600 µg). Patients with positive AHR had significantly elevated FENO and JawNO across all thresholds. The best FENO and JawNO cutoffs provided strong negative predictive values, but their positive predictive values were low. Conclusion extended nitric oxide analysis—especially FENO and JawNO—may improves the diagnostic capability of exhaled nitric oxide in predicting AHR. These findings highlight its potential as a quick, noninvasive way to rule out AHR, which could simplify asthma diagnosis and reduce the need for lengthy bronchial challenge testing.

Objective Severe asthma is biologically heterogeneous, and airway biomarkers for disease stratification remain limited. We aimed to identify a mitochondria-related induced sputum transcriptomic signature associated with severe asthma. Methods Public induced sputum microarray datasets GSE76262 (discovery) and GSE147880 (external validation) were analyzed. Mitochondrial activity was quantified by single-sample gene set enrichment analysis using MitoCarta 3.0. Severe asthma was compared with a combined non-severe asthma/healthy-control reference group. Weighted gene co-expression network analysis and LASSO logistic regression were used to derive a gene signature, followed by external validation, multivariable logistic regression, immune infiltration analysis, and nomogram construction. Results Severe asthma showed 2,000 differentially expressed genes, including 196 mitochondria-related genes. Mito Score was lower in severe asthma and discriminated severe disease (AUC, 0.791). A Mito Score-associated co-expression module yielded candidates enriched in oxidative phosphorylation, thermogenesis, cellular respiration, and reactive oxygen species-related pathways. LASSO identified a 9-gene signature (CLC, IL18R1, SLC7A11, MARCH1, RBMS2, MAN2B2, SMOX, TTC15, and CD4) with AUCs of 0.892 in discovery and 0.758 in external validation. Risk score remained independently associated with severe asthma after adjustment for age and sex. Conclusions Induced sputum transcriptomics identified a reproducible mitochondria-related 9-gene signature associated with severe asthma, supporting mitochondrial dysfunction as a clinically relevant airway feature and a candidate biomarker framework for disease stratification.

Objective Smoking relapse is prevalent, yet its long-term association with incident asthma remains underexplored. Repeated quit-relapse cycles may exacerbate airway inflammation more acutely than steady-state smoking. We investigated the association between smoking-relapse trajectories and incident asthma risk using a nationally representative longitudinal dataset. Methods We analyzed 10-year data (2009–2018) from the Korea Health Panel Survey for 16,240 adults without baseline asthma. Participants were classified into five trajectories: nonsmokers (NS), successful quitters without relapse (SQ−), successful quitters with relapse (SQ+), unsuccessful quitters with relapse (UQ+, chronic relapsers), and always smokers (AS). Cox proportional hazards models were used to estimate adjusted hazard ratios (aHRs) for incident asthma (ICD-10 J45–J46). Results During the 10-year follow-up, 159 incident asthma cases were identified. Compared to NS, chronic relapsers (UQ+) exhibited the highest risk (aHR 3.81; 95% confidence interval (CI) 1.84–7.91), followed by SQ− (aHR 2.54; 95% CI 1.30–4.96) and AS (aHR 2.25; 1.08–4.71). While UQ+ showed a higher point estimate than AS, the difference was not statistically significant. Other significant risk factors included age ≤65 years, Medical Aid enrollment, and higher comorbidity scores. Conclusions Smoking-relapse trajectories, particularly chronic relapse, are associated with an elevated risk of incident asthma. These findings should be interpreted as hypothesis-generating and require confirmation in independent cohorts.

Objective Parental numeracy skills, reflecting a quantitative domain within health literacy, may be relevant to pediatric asthma management. However, the association between parental numeracy skills and the asthma-related quality of life (QOL) of children with asthma remains insufficiently examined. This study aimed to assess the QOL of Jordanian children with asthma and to examine its association with parental numeracy skills. Methods A cross-sectional study was performed on a sample of 400 parents (66.5% mothers) of children with asthma (59.5% male) undergoing treatment at the University of Jordan Hospital. The Arabic version of the Asthma Numeracy Questionnaire (Ar-ANQ) was utilized to evaluate parental numeracy skills, while the parent-report version of the Pediatric Quality of Life Inventory (PedsQL) Asthma Module was employed to assess QOL. Quantile regression analyzed associations between parental numeracy skills, asthma control, and QOL. Results The median Ar-ANQ score was 3 (IQR: 1–4) out of 4, and the median QOL score was 60 (IQR: 50–67) out of 100. Higher parental numeracy skills were significantly associated with better asthma-related QOL among children (β = 1.99, 95% CI [0.81, 3.18], p = 0.001). Children with uncontrolled or partially controlled asthma had significantly lower QOL scores (β = −9.70, 95% CI [−15.57, −3.82], p = 0.001; β = −10.06, 95% CI [−15.83, −4.29], p = 0.001). Conclusions Higher parental numeracy skills were associated with better asthma-related QOL among children with asthma. Given the cross-sectional design, this finding should be interpreted as an association rather than evidence of a causal effect.

To the editor,The recent systematic review by Ruiduo Cheng et al.[1] evaluating the efficacy of high-flow nasal cannula and bi-level positive airway pressure in children with asthma exacerbation: a...