Allergy, Asthma & Immunology Research最新文献

{"title":"Exposure to Environmental Pollutants and the Risk of Respiratory Illnesses in 36-Month-Old Children: The Korean Children's Environmental Health Study (Ko-CHENS).","authors":"Changmin Kang, Seung-Ah Choe, Hyunseo Kim, Geunhwa Lee, JungHeum Jo, Jue Seong Lee, Dae Jin Song, Young Yoo","doi":"10.4168/aair.2026.18.5.668","DOIUrl":"10.4168/aair.2026.18.5.668","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the association of exposure to environmental pollutants and surrounding residential environments with the development of respiratory illnesses in 36-month-old children using data from the Korean CHildren's ENvironmental health Study.</p><p><strong>Methods: </strong>Demographic information and anthropometric measurements were obtained from the newborns. At 36 months of age, indoor environmental pollutant levels (particulate matter [PM₁₀ and PM_2.5], volatile organic compounds, and house dust mite allergens) were measured during home visits. Concentrations of both heavy metals (lead, mercury, and cadmium) in blood and metabolites of environmental hormones in urine were analyzed. A structured questionnaire was used to assess the presence of 6 common respiratory illnesses (infantile asthma, current asthma, recurrent wheezing, allergic rhinitis, bronchiolitis, and pneumonia) and residential environmental characteristics. Quantile-based g-computation was employed to estimate the joint association of exposure to mixtures of physical and chemical environmental factors with the risk of respiratory illnesses.</p><p><strong>Results: </strong>Among the total of 4,059 children, current allergic rhinitis was the most prevalent respiratory illness at 36 months. Compared with children without respiratory illnesses, those with respiratory illnesses showed significantly higher frequencies of exposure to environmental tobacco smoking and pet ownership. Dust mite concentrations were higher among children with recurrent wheezing and pneumonia. Mixture exposure analysis revealed that overall mixture exposure was positively associated with current allergic rhinitis, largely driven by lead and phthalate metabolites, and with pneumonia, mainly attributable to phthalate metabolites. Exposure to a mixture of multiple chemicals was positively associated with infantile asthma and current asthma.</p><p><strong>Conclusions: </strong>Direct and indirect exposures to environmental pollutants are closely associated with the development of respiratory illnesses in young children, and the surrounding residential environment during early childhood also plays a critical role in determining respiratory disease risk. These findings support the need for systematic and sustainable environmental management at both individual and community levels to protect children who are particularly vulnerable to environmental hazards.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"668-680"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in the Diagnosis and Management of Allergic Bronchopulmonary Aspergillosis/Mycosis.","authors":"Koichiro Asano, Naoki Okada, Jun Tanaka, Katsuyoshi Tomomatsu, Yoshiki Shiraishi, Tsuyoshi Oguma","doi":"10.4168/aair.2026.18.5.626","DOIUrl":"10.4168/aair.2026.18.5.626","url":null,"abstract":"<p><p>Allergic bronchopulmonary aspergillosis/mycosis (ABPA/ABPM) is an immunologically mediated pulmonary disorder triggered by the colonization of filamentous fungi in the airways of patients with asthma or cystic fibrosis, leading to type I and III hypersensitivity responses, eosinophilic mucus plug formation, and central bronchiectasis. Over the past decade, advances in basic and clinical research have substantially reshaped the understanding and management of this disease. Although <i>Aspergillus</i> species, particularly <i>Aspergillus fumigatus</i>, remain the predominant causative fungi, epidemiological studies have identified <i>Schizophyllum commune</i> as an important and previously underrecognized pathogen responsible for ABPM. A major breakthrough in elucidating disease pathophysiology is the recognition of eosinophil extracellular trap cell death as a central mechanism driving highly viscous mucus impaction. Diagnostic criteria with improved accuracy and standardized treatment protocols have been established through randomized controlled trials, culminating in the 2024 revision of the International Society for Human and Animal Mycology guidelines. However, significant unmet needs remain. Despite high initial response rates to corticosteroids or azole antifungals, nearly half of patients fail to achieve remission. Predictors of treatment failure include heightened <i>A. fumigatus</i>-specific sensitization and radiological evidence of eosinophilic mucus impaction. Biologic agents targeting type 2 inflammation have emerged as promising options for difficult-to-treat disease, although their efficacy in acute ABPA is still uncertain. Frequent exacerbations also pose a major challenge, and the potential benefits of maintenance inhaled antifungals and environmental interventions are under investigation. Collectively, advances in pathophysiology, diagnostics, and therapeutics are transforming ABPA/ABPM management, yet substantial gaps persist in improving long-term outcomes. <b>Trial Registration:</b> ClinicalTrials.gov Identifier: NCT04442269.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"626-639"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atopic Dermatitis and Sleep Disorders.","authors":"Genlong Bai, Xinyi Shao, Yi Ou, Jin Chen, Zhaofu Tan, Aijun Chen, Jingbo Zhang","doi":"10.4168/aair.2026.18.5.751","DOIUrl":"10.4168/aair.2026.18.5.751","url":null,"abstract":"<p><strong>Purpose: </strong>Atopic dermatitis (AD) is a common inflammatory skin disease affecting 129 million people worldwide and is characterized by recurrent eczema, severe pruritus, and skin barrier damage. Previous studies on AD-sleep disorder associations were limited by small sample sizes or single-center designs, lacking large-scale epidemiological evidence. This study aimed to investigate the association between AD and sleep disorders using the UK Biobank prospective cohort and to explore effects of sex, race, and obesity on this relationship.</p><p><strong>Methods: </strong>A prospective cohort design was employed, including 329,796 participants for cross-sectional analysis and 330,875 for longitudinal analysis. Multivariable logistic regression and Cox proportional hazards models were used. Subgroup and sensitivity analyses were performed to validate robustness.</p><p><strong>Results: </strong>Cross-sectional analysis showed that AD was significantly associated with increased sleep disorder risk (adjusted odds ratio, 2.84; 95% confidence interval [CI], 2.54-3.18; <i>P</i> < 0.001), while the longitudinal analysis confirmed AD as an independent predictor of sleep disorders (adjusted hazard ratio, 1.51; 95% CI, 1.32-1.73; <i>P</i> < 0.001), with Kaplan-Meier curves further demonstrating a higher cumulative risk of sleep disorders in participants with AD. Subgroup analyses revealed stronger associations in females and participants with moderate body mass index (BMI), and sensitivity analyses validated the robustness of these findings.</p><p><strong>Conclusions: </strong>AD is an independent risk factor for sleep disorders, particularly in women and individuals with moderate BMI. Future research should further explore precision-targeted therapies and management strategies for specific populations.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"751-760"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of Starting Very-Low-Dose Cow's Milk Intake in Children Aged 1-12 Years With Severe Cow's Milk Allergy: A Retrospective Study.","authors":"Kosei Yamashita, Takanori Imai, Sawa Seki, Toshiyuki Takagi, Megumi Okawa, Aiko Honda, Chihiro Kunigami, Yuki Okada, Mayu Maeda, Taro Kamiya","doi":"10.4168/aair.2026.18.5.738","DOIUrl":"10.4168/aair.2026.18.5.738","url":null,"abstract":"<p><strong>Purpose: </strong>To avoid the complete elimination of cow's milk (CM) from the diet, we introduced a very-low-dose (VLD) oral food challenge (OFC) as part of an OFC-based stepwise ingestion protocol in patients with severe CM allergy in 2019, when the OFC protocol at our center was revised. This study investigated the efficacy of initiating CM intake through an OFC-based stepwise ingestion protocol starting from a VLD in achieving a negative full-dose OFC.</p><p><strong>Methods: </strong>Patients with a history of overt allergic reactions to low-dose (LD; 3 mL CM: 100 mg CM protein) CM or lesser within 6 months and those with complete CM elimination were included. We retrospectively compared the rate of passing a full-dose OFC (200 mL CM: 6,600 mg CM protein) between patients who underwent an LD OFC before 2019 (LD group) and those who underwent a VLD OFC (0.3 mL CM: 10 mg CM protein) after 2019 (VLD group). The period for passing the full-dose OFC was evaluated using Kaplan-Meier survival analyses.</p><p><strong>Results: </strong>We allocated 270 and 267 patients into the LD and VLD groups, respectively. The median age at initiation of the OFC-based stepwise ingestion protocol was 3.6 (2.3-5.4) and 3.4 (2.0-5.1) years in the LD and VLD groups, respectively. The LD and VLD groups had CM-specific immunoglobulin E levels of 21.9 (10.9-44.0) kUA/L and 20.5 (9.0-47.2) kUA/L, respectively. The baseline clinical characteristics of the two groups showed no significant differences in background. Over 4 years, the LD and VLD groups passed the full-dose OFC at rates of 45% and 60%, respectively, with a significant difference (log-rank test, <i>P</i> = 0.023).</p><p><strong>Conclusions: </strong>Initiating CM intake through an OFC-based stepwise ingestion protocol starting from a VLD may contribute to achieving a negative full-dose OFC in patients with severe CM allergies.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"738-750"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cadherin-26 Promotes Airway Remodeling via Stabilizing Epithelial Expression of the Epidermal Growth Factor Receptor in Asthma.","authors":"Jiali Gao, Gongqi Chen, Chunli Huang, Zhen Wang, Wei Gu, Huiru Jie, Tiantian Xiong, Yuchen Feng, Lingling Yi, Dan Cheng, Guohua Zhen","doi":"10.4168/aair.2026.18.5.702","DOIUrl":"10.4168/aair.2026.18.5.702","url":null,"abstract":"<p><strong>Purpose: </strong>Activation of epidermal growth factor receptor (EGFR) signaling in airway epithelial cells leads to epithelial-mesenchymal transformation (EMT) and airway remodeling in asthma. However, the mechanism regulating EGFR expression is not fully understood. We hypothesized that cadherin-26 (CDH26), a highly expressed cadherin in airway epithelium, promotes airway remodeling via regulating EGFR signaling in asthma.</p><p><strong>Methods: </strong>The expression of CDH26 in airway brush cells of asthmatic patients was examined using quantitative polymerase chain reaction. Airway hyperresponsiveness and remodeling were assessed in the house dust mite (HDM)-sensitized and -challenged <i>Cdh26</i>-deficient mice. The role and mechanism of CDH26 in epidermal growth factor (EGF)-induced EMT were measured in cultured human bronchial epithelial BEAS-2B cells.</p><p><strong>Results: </strong>The expression of CDH26 in airway brush cells was significantly correlated with the thickness of airway basement membrane in asthma patients. <i>Cdh26</i> deficiency significantly reduced airway hyperresponsiveness and remodeling in HDM-sensitized and -challenged mouse model. In cultured human bronchial epithelial BEAS-2B cells, CDH26 knockdown inhibited EGF-induced EMT, whereas overexpression of CDH26 promoted EGF-induced EMT. Furthermore, CDH26 knockdown suppressed EGF-induced activation of EGFR signaling including phosphatidylinositol 3-kinase and AKT phosphorylation. By contrast, CDH26 overexpression intensified EGF-induced activation of EGFR signaling. Mechanistically, CDH26 knockdown promoted the proteasomal degradation of the EGFR.</p><p><strong>Conclusions: </strong>CDH26 promoted airway remodeling via stabilizing the epithelial expression of EGFR and sustaining the activation of EGFR signaling in asthma. Thus, CDH26 can be a potential therapeutic target for airway remodeling in asthma.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"702-720"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-Wide Risk Assessment and Clinical Prediction of Iodinated Contrast Media-Induced Anaphylaxis.","authors":"Soo Jie Chung, Eunsoon Shin, Yong-Seok Kim, So-Hee Lee, Sun-Sin Kim, Sun Young Paik, Heung-Woo Park, Sae-Hoon Kim, Sungwon Jeon, Jong Bhak, Hye-Ryun Kang, Yoon-Seok Chang","doi":"10.4168/aair.2026.18.5.776","DOIUrl":"10.4168/aair.2026.18.5.776","url":null,"abstract":"<p><strong>Purpose: </strong>Iodinated contrast media (ICM) are widely used in diagnostic imaging, but may trigger immediate hypersensitivity reactions, including anaphylaxis. Although human leukocyte antigen (HLA) associations have been proposed, genome-wide evidence remains limited. To identify genetic risk variants associated with ICM-induced anaphylaxis and evaluate their clinical utility.</p><p><strong>Methods: </strong>We conducted a genome-wide association study (GWAS) in 91 Korean patients with confirmed ICM-induced anaphylaxis (discovery, n = 67; replication, n = 24) and 1,565 controls. Genotyping used a Korean-specific single nucleotide polymorphism (SNP) array. Significant variants were replicated. HLA alleles were imputed in the combined dataset. Linkage disequilibrium (LD) among significant loci was analyzed. Cumulative genetic burden was assessed by summing risk alleles per individual. A Least Absolute Shrinkage and Selection Operator-based prediction model incorporated genetic and clinical variables.</p><p><strong>Results: </strong>Nineteen SNPs reached genome-wide significance and were replicated, including rs2229629 in <i>HK2</i> (odds ratio, 5.02; <i>P</i> = 9.6 × 10⁻²³), suggesting altered glycolysis. Additional variants were found near <i>GABBR1, ZNF391, ATAT1</i>, and <i>HLA</i> genes. Imputed HLA-DRB1*15:02 was significantly enriched in patients (41.8% <i>vs.</i> 5.9%, <i>P</i> = 5.21 × 10⁻¹⁷). LD analysis showed haplotypic clustering within HLA and non-HLA loci. A gene dosage effect was observed. The combined genetic-clinical model showed the highest predictive performance (area under the curve [AUC] = 0.888), exceeding genetic (AUC = 0.800) and clinical (AUC = 0.835) models.</p><p><strong>Conclusions: </strong>This first GWAS of ICM-induced anaphylaxis identifies susceptibility loci across metabolic, immune, and neuroimmune pathways. <i>HK2</i> was most strongly associated, and HLA-DRB1*15:02 was robustly replicated.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"776-792"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Phenotyping Based on Blood Transcriptome-Associated Clusters in Asthma: Findings From Two Korean Asthma Cohorts.","authors":"Eunse Kim, So-Young Park, Byung Keun Kim, Min-Hye Kim, Ji-Yong Moon, Jong Eun Lee, Hye Yoon Jang, Eunsoon Shin, Jae-Woo Jung, Taehoon Lee, Chan Sun Park, Jeong-Hee Choi, Sujeong Kim, Sang-Hoon Kim, Hye-Kyung Park, Sae-Hoon Kim, Sang-Ha Kim, Joo-Hee Kim, Jae-Woo Kwon, Young-Joo Cho, Byung-Jae Lee, Ian M Adcock, Kian Fan Chung, Sungho Won, Tae-Bum Kim","doi":"10.4168/aair.2026.18.5.652","DOIUrl":"10.4168/aair.2026.18.5.652","url":null,"abstract":"<p><strong>Purpose: </strong>Asthma is heterogeneous in its molecular and clinical manifestations, complicating treatment. In this study, we investigated the molecular phenotypes of asthma using RNA-sequencing (RNA-seq) of peripheral blood mononuclear cells to advance precision medicine approaches.</p><p><strong>Methods: </strong>We analyzed peripheral blood RNA-seq data from 456 participants from the Cohort for Reality and Evolution of Adult Asthma in Korea, including 23 patients with severe asthma and 433 with non-severe asthma to identify blood transcriptome-associated clusters (B-TACs) that correlate with distinct inflammatory processes. This included a meta-analysis of differentially expressed genes to refine gene selection for defining B-TACs. Gene Set Variation Analysis was used to assess the differential activation of biological pathways across B-TACs. We validated these findings in the Precision Medicine Intervention in Severe Asthma cohort of 122 patients, focusing on cluster stability, clinical correlates, and treatment responsiveness.</p><p><strong>Results: </strong>Our analysis identified 3 B-TACs (B-TAC1, B-TAC2 and B-TAC3) with B-TAC1 and B-TAC2 showing higher blood eosinophil levels than B-TAC3. B-TAC1 was characterized by a clear T2-high inflammatory profile, whereas B-TAC2 exhibited a mixed molecular phenotype with both T2-high and non-T2 features. B-TAC3 was associated with low T2 and inflammasome-related inflammation profiles. Validation using the PRISM cohort underscored the stability of B-TAC1 and B-TAC2. Notably, patients with B-TAC2 molecular phenotype had lower biologics use and tended to have less favorable treatment outcomes than those with B-TAC1.</p><p><strong>Conclusions: </strong>We discovered and validated 3 B-TACs, with B-TAC2 displaying a mixed T2-high and non-T2 phenotype, suggesting a potential reduction in responsiveness to biologic treatments. These findings provide molecular insights that may guide the development of personalized treatment strategies for asthma.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"652-667"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated RNA-Seq Profiling Identifies NRXN1+ Cell-Fibroblast Associated MAPK Signaling in Prurigo Nodularis.","authors":"Jiyun Jang, Young-Bok Lee, Hwee-Seon Park, Narang Hong, Hyung Don Kook, Hye Jung Jung, Jong-Il Kim, Jiyoung Ahn","doi":"10.4168/aair.2026.18.5.761","DOIUrl":"10.4168/aair.2026.18.5.761","url":null,"abstract":"<p><strong>Purpose: </strong>Prurigo nodularis (PN) is chronic pruritic dermatosis with hyperkeratotic nodules and persistent itch, occurring alone or with atopic dermatitis (AD). The molecular basis of nodular architecture and sustained pruritus remain poorly defined, particularly the role of fibroblasts and their interactions with neuronal components. This study aimed to identify PN-specific pathogenic profiles by comparing lesional transcriptomes from AD, atopic prurigo (AP), and PN.</p><p><strong>Methods: </strong>Bulk RNA sequencing was performed on lesional skin from AD (n = 6), AP (n = 7), PN (n = 7), and healthy controls (HC; n = 4). Publicly available single-cell RNA-sequencing datasets were reanalyzed for cell-type signatures. Integrated analyses included differentially expressed genes, pathway enrichment, cell-type deconvolution, ligand-receptor inference, and immune cell profiling.</p><p><strong>Results: </strong>PN lesions showed MAPK/ERK pathway enrichment in fibroblasts compared with AD and AP. NRXN1+ cells were inferred as major interacting partners of fibroblasts, with ligand-receptor interactions consistent with enhanced fibroblast MAPK/ERK activity. Immune pathway analyses showed weaker Th2 pathway activity in PN compared with AD/AP, providing context for neuronal-stromal interactions as a putative distinguishing feature.</p><p><strong>Conclusions: </strong>PN shows enhanced MAPK/ERK pathway enrichment in fibroblasts and inferred NRXN1+ cell-fibroblast interactions. This candidate axis may contribute to nodular lesion architecture and persistent pruritus, suggesting potential therapeutic strategies.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"761-775"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F1-Activated lncRNA FTX Promotes Asthma Progression via Regulating the SRSF1/RBPJ Axis.","authors":"Yuting Lai, Guoqing Qiu, Na Li, Yuming Chen, Yan Shen","doi":"10.4168/aair.2026.18.5.681","DOIUrl":"10.4168/aair.2026.18.5.681","url":null,"abstract":"<p><strong>Purpose: </strong>Long non-coding RNA five prime to Xist (FTX) is considered a regulator for asthma. Therefore, we aimed to explore its more roles and molecular mechanisms in asthma process.</p><p><strong>Methods: </strong>Serum samples from controls and asthmatics were collected. Asthma mouse models were induced with ovalbumin (OVA), and cell models were established using airway smooth muscle cells (ASMCs) treated with platelet-derived growth factor BB (PDGF-BB). The inspiratory and expiratory airway resistances of mice were examined by measuring airway hyperresponsiveness. The pathological changes of mice lung tissues were observed by hematoxylin & eosin, periodic acid-Schiff, and Masson staining. Serum immunoglobulin E and inflammatory factor levels were detected using an enzyme-linked immunosorbent assay. The CCK-8, Transwell, and flow cytometry were used to assess cell function. FTX, E2F family transcription factor 1 (E2F1), serine rich/arginine splicing factor 1 (SRSF1), and recombination signal binding protein J (RBPJ) levels measured by quantitative real-time-polymerase chain reaction or Western blotting. The relationships among FTX, E2F1, SRSF1, and RBPJ were evaluated by dual-luciferase report, ChIP, RNA pull-down and RIP assay. The effect of FTX/SRSF1 on RBPJ mRNA stability was analyzed by the actinomycin D treatment assay.</p><p><strong>Results: </strong>Upregulated FTX was detected in asthmatic patients, asthma mice, and PDGF-BB-induced ASMCs. FTX downregulation repressed PDGF-BB-induced ASMCs viability, migration, and inflammation. E2F1 bound to the FTX promoter region to activate its expression, and E2F1 downregulation could repress PDGF-BB-induced ASMCs function via reducing FTX expression. Also, FTX stabilized RBPJ mRNA by interacting with SRSF1. RBPJ overexpression reversed the downregulation effect of FTX knockdown on PDGF-BB-induced ASMCs viability, migration, and inflammation. Meanwhile, E2F1 downregulation alleviated mouse asthma symptoms by inhibiting the FTX/SRSF1/RBPJ pathway.</p><p><strong>Conclusions: </strong>FTX, transcriptionally activated by E2F1, promoted asthma progression via the the regulation of the SRSF1/RBPJ pathway, thereby providing a possible therapeutic target for asthma treatment that warrants further validation.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"681-701"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between C-Reactive Protein-Triglyceride Glucose Index and All-Cause Mortality and Exacerbation in Adult Asthma: NHANES, 1999-2010 and 2015-2018.","authors":"Jiaye Wang, Miaomiao Zhao, Hao Chen, Shiyu Hu, Chengshui Chen, Yingqing Zhang, Wenyu Chen","doi":"10.4168/aair.2026.18.5.721","DOIUrl":"10.4168/aair.2026.18.5.721","url":null,"abstract":"<p><strong>Purpose: </strong>This study investigates the association between the C-reactive protein-triglyceride-glucose index (CTI), indicative of systemic inflammation and insulin resistance, and all-cause mortality as well as asthma exacerbations in adults with asthma.</p><p><strong>Methods: </strong>Data from eight cycles of the US National Health and Nutrition Examination Survey (1999-2010 and 2015-2018) were analyzed. Adults aged ≥ 20 years were included, excluding those who were missing key variables. This resulted in 13,972 participants, of whom 1,832 had asthma. Participants were grouped into CTI tertiles. Participants self-reported exacerbations, and survival status was linked with the National Death Index. Complex survey weighting was applied to ensure national representativeness. Weighted multivariate logistic regression and Cox proportional hazards models assessed associations while adjusting for demographics, socioeconomic factors, body mass index, smoking, alcohol consumption, comorbidities, and laboratory indicators.</p><p><strong>Results: </strong>The fully adjusted model revealed no significant association between CTI and asthma prevalence (odds ratio [OR], 1.07; 95% confidence interval [CI], 0.99-1.16; <i>P</i> = 0.078) but showed a strong association with all-cause mortality (hazard ratio [HR], 1.43; 95% CI, 1.12-1.81; <i>P</i> = 0.004). Patients in the highest CTI tertile exhibited a more than two-fold higher risk of mortality compared to those in the lowest tertile (HR, 2.22; 95% CI, 1.24-3.98; <i>P</i> = 0.007). Furthermore, higher CTI was associated with asthma exacerbation (OR, 1.23; 95% CI, 1.01-1.50; <i>P</i> = 0.039).</p><p><strong>Conclusions: </strong>In this nationally representative sample, higher CTI was associated with higher all-cause mortality and higher odds of recent asthma exacerbations among adults with asthma, while no significant association with asthma prevalence was observed. CTI may help inform prognostic stratification in asthma and prospective studies are warranted.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 5","pages":"721-737"},"PeriodicalIF":4.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}