Journal of Asthma最新文献

Objective: Home environmental asthma assessment and trigger management are critical in pediatric asthma care, particularly in underserved rural areas. However, in-person home assessments are often logistically, financially, and culturally challenging. This study developed a video-based virtual simulation designed to train nursing students and community health workers (CHWs) to conduct remote (virtual) asthma home environmental assessments.

Methods: It was developed at Samford University's Experiential Learning and Simulation Center, guided by the NLN/Jeffries Simulation Theory. The authors established clear learning objectives, designed the simulation, created a scenario, and incorporated structured pre- and post-simulation debriefings. Key environmental triggers, selected from the Environmental Protection Agency (EPA) Home Environmental Assessment Checklist, included dust, mold, cigarette smoke, cleaning supply irritants, pets, and pests, all of which were represented in the simulation lab. The recorded simulation was distributed to simulation education partners and practicing asthma educators (AE-Cs) for expert evaluation using a standardized feedback form to refine the program. The simulation was developed and evaluated between January and May 2024.

Results: A total of 12 experts in nursing education, asthma education, and simulation reviewed the simulation. Their average ratings were: learning objectives 4.73, content clarity 4.95, engagement 4.53, realism 4.65, effectiveness in promoting learning 4.8, and technology utilization 4.9. The overall evaluation score was 4.9 out of 5.

Conclusion: Expert evaluation indicated high content validity and strong perceived educational value for preparing nursing students and CHWs to conduct remote asthma home environmental assessments. Further research is needed to evaluate learner outcomes.

Background: Obesity-related asthma (OB-AS) is characterized by a suboptimal response to standard therapies and an elevated risk of refractory asthma. While caffeine demonstrates protective associations against both asthma and obesity, its role in OB-AS remains unclear.

Methods: A cross-sectional study was conducted using data from the National Health and Nutrition Examination Survey (2007-March 2020). Weighted multiple regression and restricted cubic spline models were employed to assess the relationship between caffeine intake and OB-AS risk. A two-sample Mendelian randomization (MR) analysis was performed to elucidate the causal relationship between coffee consumption and OB-AS risk, followed by a mediation analysis to examine the gut microbiota's role. Additionally, core genes of caffeine's effect on OB-AS were identified to explore underlying biological mechanisms.

Results: After screening, 3751 asthma cases and 27,935 non-asthma controls were included. Caffeine intake was inversely correlated with OB-AS risk (odds ratio [OR] = 0.83, 95% confidence interval [CI] = 0.70-0.97, p = 0.020). A significant non-linear association between caffeine intake and OB-AS risk was observed among males (P for non-linearity = 0.009). MR analysis confirmed a causal association between coffee consumption and reduced OB-AS risk (inverse-variance weighted method: OR = 0.133, 95% CI = 0.025-0.712, p = 0.019). Mediation analysis revealed that Collinsella mediated 14.9% of this association. We identified 42 core genes associated with caffeine's effect on OB-AS, with enrichment observed in corticosteroid response pathways.

Conclusions: Caffeine intake demonstrates a protective effect against OB-AS risk, partially mediated by Collinsella. It is hypothesized that caffeine might influence OB-AS via corticosteroid response pathways.

Objective: An accurate understanding of asthma exacerbation frequency is essential for optimal management. However, discrepancies may exist between patient-reported and clinically documented exacerbations. This study aimed to investigate the characteristics and associated factors of these discrepancies.

Methods: We retrospectively reviewed consecutive patients who regularly visited our hospital for asthma treatment between January 2019 and April 2024 and were followed for one year. Severe exacerbations were defined as short bursts (SB) of systemic corticosteroids lasting ≥3 days or doubling of maintenance oral corticosteroid dose for ≥3 days. Patients were categorized into concordant, under-reporting, or over-reporting groups based on the discrepancies between patient-reported and chart-documented SB counts.

Results: Data from 289 patients were analyzed. The level of concordance was weak (κ = 0.26). Among them, 11.4% under-reported and 4.1% over-reported SB events. Among those with objectively confirmed SB, nearly three-quarters under-reported their SB frequency, and over 30% under-reported by at least two episodes. Multivariate analysis revealed that younger age, Global Initiative for Asthma (GINA) step 5, and lower asthma control test (ACT) scores were independently associated with under-reporting by at least one episode (OR = 0.66, 95% CI 0.47-0.93, per 10-year increase; OR = 5.22, 95% CI 1.76-15.01; OR = 0.89, 95% CI 0.80-0.98, per 1-unit ACT increase). Over-reporting was also associated with GINA step 5 and lower ACT scores.

Conclusions: A notable proportion of patients exhibited misperception regarding their annual frequency of asthma exacerbations. Particular attention should be paid to patients with severe or poorly controlled asthma, who are more likely to misreport exacerbation events.

Objective: To investigate the protective effect of N-acetylcysteine (NAC) against benzo[a]pyrene (BaP)-aggravated lung injury in asthma and to elucidate whether it is mediated through the ROS/CREB/ERK signaling pathway.

Methods: Twenty-four BALB/c mice were randomly divided into Control, Model (OVA + BaP), and Intervention (OVA + BaP + NAC) groups. An aggravated asthma model was established by ovalbumin (OVA) sensitization/challenge combined with intratracheal instillation of BaP. The NAC group received NAC via gavage. Airway inflammation and mucus secretion were assessed by H&E and PAS staining. Serum IgE levels were measured by ELISA. SOD activity and MDA content were detected using commercial kits. ROS levels in lung tissue were observed by fluorescence staining. The mRNA expression of mucin genes (MUC5AC, MUC5B, MUC16, etc.) was detected by qPCR. The protein expression of apoptosis-related markers (Bax, Bcl-2) and signaling pathway components (p-ERK1/2, p-CREB) was measured by Western Blot.

Results: Compared with the Model group, NAC intervention significantly alleviated airway inflammatory cell infiltration, mucus hypersecretion, and epithelial damage, and reduced serum IgE levels. Meanwhile, NAC effectively decreased ROS and MDA levels, increased SOD activity in lung tissue, reversed the BaP-induced upregulation of MUC5AC, MUC5B, and MUC16 genes, and modulated the Bax/Bcl-2 ratio to inhibit apoptosis. Mechanistically, NAC significantly inhibited BaP-induced phosphorylation of ERK1/2 and CREB.

Conclusion: NAC can mitigate BaP-induced airway mucus hypersecretion and apoptosis, thereby alleviating asthma lung injury, by scavenging ROS and inhibiting the overactivation of the ROS/CREB/ERK signaling pathway. This study provides experimental evidence supporting NAC as a potential therapeutic strategy for preventing and treating air pollution-associated asthma.

Background: A subset of patients with asthma develops persistent airflow limitation (PAL) despite optimal treatment. The role of small airways dysfunction (SAD) in this phenotype, and its relationship with symptoms, remains incompletely understood.

Objectives: To assess small airways function in asthmatic patients with PAL and compare it with patients with fully reversible asthma and with COPD; and to explore correlations between small airway indices and patient-reported outcomes.

Methods: We enrolled 60 patients (20 with asthma and PAL, 20 with fully reversible asthma, 20 with COPD) matched for age, sex, and pre-bronchodilator FEV1. Small airways function was evaluated using impulse oscillometry (IOS; R5-R20) and single-breath nitrogen washout test (SBNWT; dN2). Patients completed a daily symptom diary (dyspnea, cough, sputum, and rescue medication use) over four weeks.

Results: Compared with fully reversible asthma, asthmatic patients with PAL showed significantly higher dN2 and R5-R20 values, though less pronounced than in COPD. SAD (R5-R20 > 0.07 kPa·L^-1·s) was present in all COPD patients, 79% of PAL patients, and 37% of reversible asthma patients (p < 0.001). In PAL, R5-R20 correlated strongly with dyspnea scores (r = 0.64, p < 0.001). In reversible asthma, R5-R20 correlated with cough and rescue medication use, whereas in COPD, symptoms were primarily related to residual volume.

Conclusions: Small airways dysfunction is highly prevalent in asthmatic patients with PAL and significantly contributes to daily symptom burden. Its intermediate severity between COPD and reversible asthma suggests that SAD plays a central role in the pathogenesis of fixed obstruction, suggesting a potential role for targeted diagnostic and therapeutic strategies.

Objective: Allergic asthma (AAS) affects over 300 million people globally, creating significant health and economic challenges. Belamcanda chinensis (L.) DC, known as SG, is traditionally used in the "Shegan-Mahuang decoction" for AAS treatment, yet its separate therapeutic effects are underexplored. This study aims to investigate the anti-AAS properties of isoflavones derived from SG.

Methods: Using a mouse model induced by house dust mite (HDM), the research involved treating HDM-sensitized mice with tectorigenin, dexamethasone, and varying doses of SG (low, medium, and high). Anti-inflammatory effectiveness was assessed through assays measuring cytokines, along with histological techniques such as hematoxylin-eosin and periodic acid-Schiff staining, alongside leukocyte counts. Additionally, gas chromatography-mass spectrometry was utilized to analyze tissue metabolic changes.

Results: The medium dose of SG (435 mg/kg) significantly diminished inflammatory cell infiltration, goblet cell hyperplasia, and mucus production. Furthermore, SG treatment reduced cytokine levels and inflammatory cells in bronchoalveolar lavage fluid and lowered serum HDM-IgE and total IgE levels, showcasing a notable reduction in inflammation. The metabolic profile of lung tissue from SG-treated mice closely resembled that of dexamethasone-treated mice, with levels of seven amino acid-related metabolites normalizing, aligning with decreased inflammatory responses.

Conclusions: This study highlights the potential of SG isoflavone extract as an effective therapeutic strategy for AAS, shedding light on the mechanisms through which SG may alleviate allergic asthma symptoms.

Objective: Asthma is a heterogeneous disorder in which a subset of patients exhibits a type 2 (Th2- or T2-high) endotype driven by eosinophilic, IL-4/IL-13-mediated inflammation. Traditional animal and 2D cell-based models incompletely reproduce human airway immune responses, particularly the Th2 phenotype. To address this gap, we developed a three-dimensional (3D) ex vivo model of human nasal respiratory mucosa incorporating type-2-biased immune stimulation.

Methods: Primary nasal mucosal biopsies were expanded under air-liquid interface (ALI) conditions and either exposed to IL-4/IL-13 or co-cultured with autologous polarized CD4+ Th2 lymphocytes and dendritic cells to generate a Th2-dominated microenvironment. Tissue morphology and barrier function were monitored longitudinally by phase-contrast microscopy and transepithelial electrical resistance (TEER).

Results: Induction of a type-2 inflammatory state was confirmed by increased secretion of periostin, STAT-6, IL-4 and IL-13 in apical and basal compartments, together with modest TEER reduction and evidence of epithelial remodeling, whereas IL-8 and chitinase family proteins did not increase, thereby excluding a COPD-like or type-2-low phenotype.

Conclusions: Rather than fully recapitulating clinical asthma, this methodological model reproduces key immunopathologic features of T2-high airway inflammation in a patient-derived 3D context. It provides a stable, human-relevant platform for mechanistic studies and for future preclinical screening of targeted anti-inflammatory therapies.

Objective: Effective pediatric asthma management relies on medication adherence, correct inhaler technique, and positive parental illness perception. This study examined the levels, interrelationships, and predictive value of these factors for asthma control among children aged 7-11 years.

Methods: In this cross-sectional observational study, 62 children with asthma and their caregivers were recruited from community and clinical settings in Alabama, USA. Asthma control was assessed using the Childhood Asthma Control Test (C-ACT), medication adherence via the Medication Adherence Report Scale for Asthma (MARS-A), and parental illness perception via the Asthma Illness Representation Scale (AIRS), including five subscales: Attitudes Toward Medication Use, Treatment Expectations, Facts About Asthma, and Nature of Symptoms/Emotional Aspects. Inhaler technique was evaluated using a pressurized metered-dose inhaler (pMDI) with a spacer via a 9-step checklist. Descriptive statistics summarized outcomes, and correlations and regressions explored relationships.

Results: Only 34.77% of participants demonstrated correct inhaler technique. Inhaler technique correlated positively with asthma control (r_s = .25, p = .048), and medication adherence correlated with parental attitudes toward medication (r_s = .46, p < .001). Regression showed that later age at diagnosis predicted poorer asthma control (B = -0.64, p = .008). Ordinal regression indicated that higher caregiver education (high school: B = -5.73, p = .019; college: B = -4.90, p = .027) and perceiving income as exceeding expenses (B = -4.63, p = .045) were associated with better asthma control.

Conclusions: Despite favorable control scores, incorrect inhaler use and suboptimal adherence remain challenges. Parental perceptions and sociodemographic factors, particularly education and financial well-being, significantly influence outcomes. Findings underscore the need for family-centered educational strategies to improve pediatric asthma management.

Objective: Our primary objective was to evaluate the interrater reliability (IRR), responsiveness and predictive validity of two asthma severity scores in obese and normal weight (NW) children. Our secondary objective was to compare asthma interventions in these groups.

Methods: This was a planned secondary analysis of a prospective observational study of children aged 2-to- < 18 years treated for asthma exacerbations in the emergency department. Obesity was defined as >95th% sex-specific weight-for-age. Clinicians completed paired assessments of the Asthma Clinical Score (ACS) and Pediatric Respiratory Assessment Measure (PRAM). IRR was analyzed using Cohen's kappa coefficient. Reliable change index was used to determine the responsiveness. Predictive validity of the pretreatment ACS and PRAM was analyzed using Receiver Operating Characteristics and Akaike Information Criterion. The likelihood of receiving an intervention was described using odds ratios (OR).

Results: 399 Children were enrolled, 111 classified as obese. In obese children, the ACS showed moderate IRR, while the PRAM showed weak IRR (κ_w 0.73 and 0.57, respectively). Both scores better detected responsiveness in NW versus obese children (ACS 34% vs 23%, PRAM 28% vs 3.7%, respectively) but were better predictors of hospitalization in obese children (ACS 0.85, vs 0.74 and PRAM 0.79 vs 0.72, respectively). Obese children had higher odds of receiving intravenous methylprednisolone, continuous albuterol, and noninvasive ventilation.

Conclusion: Performance of the ACS and PRAM varied between obese and NW children. Future studies should aim to fully elucidate the performance and utility of asthma severity scores in obese children.