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Background: Although asthma does not appear to be a risk factor for severe coronavirus disease 2019 (COVID-19), outcomes could vary for patients with different asthma subtypes. The objective of this analysis was to compare COVID-19 outcomes in real-world cohorts in the United States among patients with asthma, with or without evidence of allergy.Methods: In a retrospective analysis of the COVID-19 Optum electronic health record dataset (February 20, 2020-January 28, 2021), patients diagnosed with COVID-19 with a history of moderate-to-severe asthma were divided into 2 cohorts: those with evidence of allergic asthma and those without (nonallergic asthma). After 1:1 propensity score matching, in which covariates were balanced and potential bias was removed, COVID-19 outcomes were compared between cohorts.Results: From a COVID-19 population of 591,198 patients, 1595 patients with allergic asthma and 8204 patients with nonallergic asthma were identified. After propensity score matching (n = 1578 per cohort), risk of death from any cause after COVID-19 diagnosis was significantly lower for patients with allergic vs nonallergic asthma (hazard ratio, 0.48; 95% CI 0.28-0.83; P = 0.0087), and a smaller proportion of patients with allergic vs nonallergic asthma was hospitalized within - 7 to + 30 days of COVID-19 diagnosis (13.8% [n = 217] vs 18.3% [n = 289]; P = 0.0005). Among hospitalized patients, there were no significant differences between patients with allergic or nonallergic asthma in need for intensive care unit admission, respiratory support, or COVID-19 treatment.Conclusions: Asthma subtype may influence outcomes after COVID-19; patients with allergic asthma are at lower risk for hospitalization/death than those with nonallergic asthma. [ABSTRACT FROM AUTHOR]

Background: In the United States, dupilumab is approved for moderate-to-severe eosinophilic or oral corticosteroid-dependent asthma, and omalizumab is approved for managing moderate-to-severe allergic asthma uncontrolled by inhaled corticosteroids. However, limited comparative effectiveness data exist for these biologics due to differing patient characteristics and treatment histories., Objective: This study assessed the real-world effectiveness of dupilumab and omalizumab for asthma in patients in the United States., Methods: In this retrospective observational study, TriNetX Dataworks electronic medical record data were used to identify patients with asthma age ≥12 years who initiated (index) dupilumab or omalizumab between November 2018 and September 2020 and who had at least 12 months of pre- and post-index clinical information. Inverse probability of treatment weighting was applied to balance potential confounding in treatment groups. Asthma exacerbation rates and systemic corticosteroid (SCS) prescriptions were compared using a doubly robust negative binomial regression model, adjusting for baseline exacerbation/SCS rates and patient characteristics with ≥10% standardized differences after inverse probability of treatment weighting., Results: All inclusion and exclusion criteria were met by 2138 dupilumab patients and 1313 omalizumab patients. After weighting, the majority of baseline characteristics were balanced (standard difference <10%) between the 2 groups. Dupilumab was associated with a 44% lower asthma exacerbation rate (P < .0001) versus omalizumab. Additionally, dupilumab treatment significantly (P < .05) reduced SCS prescriptions by 28% during the follow-up period compared with omalizumab treatment., Conclusions: The US ADVANTAGE real-world study demonstrated a significant reduction in severe asthma exacerbations and SCS prescriptions for patients prescribed dupilumab compared with patients prescribed omalizumab during 12 months of follow-up., Competing Interests: Disclosure statement This research was sponsored by Sanofi and Regeneron Pharmaceuticals, Inc. Disclosure of potential conflict of interest: E. Bleecker reports potential conflicts with Sanofi, AstraZeneca, Novartis, and Regeneron. M. Blaiss reports potential conflicts with Sanofi, Regeneron, Amgen, and Lanier Biotherapeutics. J. Jacob-Nara is an employee of Sanofi. K. Borsos, A. Nag, and R. Nair were employees of Sanofi at the time of study and preparation of manuscript. Z. Wang and X. Soler are employees and stockholders of Regeneron. L. Huynh, M. Sheng Duh, T. Guo, and M. Ye are employees of Analysis Group, Inc., which received research funds from Sanofi to conduct this study. R. H. Stanford is a paid consultant for Sanofi., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: IL-35 is an inhibitory cytokine, produced by Treg cells, smooth muscle cells, monocytes and vascular endothelial cells and has multiple functions to produce various phenotypic features. The aim of current study was to investigate the role of serum IL-35 concentration and other clinical parameters in allergic asthma patients and the role of treatment with corticosteroids on IL-35 concentration. Patients and methods: Clinical samples were obtained with informed consent from 54 allergic asthma patients (32 with treatment and 22 without treatment), 14 patients with Helicobacter pylori (H. pylori) infection and 22 healthy controls. The serum IL-35 has been detected according to the manufacturer’s instruction with commercial human IL-35 ELISA Kit (My biosource, USA). Results: The mean concentration of plasma IL-35 in allergic asthma patients with treatment, allergic asthma patients without treatment, healthy control, and H. pylori patients, were 35.34, 71.4, 94.5 and 68.1pg/ml, respectively, and the highest concentrations were 104.62, 310.3, 241.3, and 229.1pg/ml, the lowest concentrations were 9.10, 11.6, 29.1, and 19.3pg/ml, respectively, and no significant correlations were found between IL-35 levels and total serum IgE levels, white blood cell count, and the percentage of eosinophils count in two groups of patients. Conclusion: This study supported previous studies in that serum IL-35 level is reduced in allergic asthma patients. [ABSTRACT FROM AUTHOR]

Objective: Allergic asthma is a growing burden on national public health services due to its high prevalence. The aim of this experiment was to investigate whether miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice through the regulation of target genes., Methods: Screening for differentially expressed miRNAs in asthma model mice was carried out by constructing a mouse model of allergic asthma. qRT-PCR was performed to determine candidate miRNAs in each group of bronchial tissues. Western blot detection of the expression levels of predicted candidate target genes in each group of bronchial tissues was conducted. A dual luciferase assay was performed to validate the binding of miR-26a-5p to target genes. Fibronectin, a marker of cellular fibrosis, was detected via flow cytometry. CCK8 and BrdU staining were used to detect the proliferation ability of each group of cells., Results: miR-26a-5p is able to target and bind to ABL2 3'-UTR, MMP16 3'-UTR and PDE7A 3'-UTR sequences. After interference with miR-26a-5p, improved bronchial histopathology and reduced peribronchial collagen deposition were found. Compared with the model group, interference with miR-26a-5p reduced lung fibrosis, decreased fibroblasts and increased apoptosis in mouse bronchial tissues; overexpression of miR-26a-5p decreased apoptosis in mouse bronchial tissues. Compared with the model group, the serum levels of IL-4, IL-5, IL-13 and I IFN-γ were decreased in the miR-26a-5p inhibitor group and increased in the miR-26a-5p mimic group. The immunohistochemical results showed that the expression of ABL2, MMP16 and PDE7A was significantly reduced after intervention with miR-26a-5p. Compared with the model group, the apoptosis rate of cells in the miR-26a-5p inhibitor group of the allergic asthma model was upregulated, the levels of IL-4, IL-5, IL-13, IFN-γ and ROS were decreased, the expression of the miRNA and proteins of ABL2, MMP16 and PDE7A was decreased, the expression of LC3A and P62 was significantly increased and the expression of LC3B, Beclin1, Atg5 and fibrosis markers collagen I and α-SMA was decreased., Conclusion: miR-26a-5p affects cellular fibrosis and thus airway remodeling in asthmatic mice by regulating target genes.

Objective. Bisphenol A (BPA) is being increasingly associated with adverse health effects. Our objective was to determine whether urinary BPA concentration is associated with allergic asthma in a representative US population. Methods. Data for this analysis were obtained from the National Health and Nutrition Examination Survey 2005-2006 survey and included asthma-related questions, total immunoglobulin E (IgE), 19 allergen-specific IgE levels, and urinary environmental phenol measurements. Allergic asthma was defined as a history of asthma ever, high eosinophil count, and high total IgE or atopy. Association analyses included dichotomous and polychotomous logistic regression, receiver operating characteristic curves, Akaike information criterion, and likelihood ratio χ2. Results. We found that 10-fold increase in BPA was independently associated with a higher likelihood of allergic asthma in females [odds ratio (OR)  =  2.21, p = .032] but not in males (OR =  0.83, p = .474). These findings were reaffirmed when allergic asthma was defined based on atopy rather than total IgE (OR  = 2.45, p = .001 in females and OR  =  0.83, p = .605 in males). Urinary BPA was significantly associated with sensitization to various specific allergens in a dose-response manner. Lastly, urinary BPA independently predicted an asthma episode in the past 12 months in females but not in males. Conclusions. Urinary BPA is significantly associated with allergic asthma in females. [ABSTRACT FROM AUTHOR]

Allergen immunotherapy (AIT) is the only disease-modifying treatment approved for allergic rhinitis and allergic asthma and represents a suitable therapeutic option, especially in childhood, to modify the progression of respiratory allergic diseases. Starting from the previous “generic class effect” evaluation, as testified by the numerous meta analyses, AIT is now considered a product-specific pathogenic-oriented treatment. Background: AIT was empirically proposed more than one century ago in the subcutaneous form (SCIT), but the IgE-mediated mechanism of allergy was elucidated only after 50 years of clinical use of the treatment. The sublingual administration (SLIT) was developed during the 1980 ties, to achieve an improvement in safety and convenience. While SCIT is approved in the United States for the treatment of asthmatic patients with more than 12 years, so far few trials evaluated the clinical efficacy and safety of SLIT in children with allergic asthma, although the indications and some aspects remain unclear. Certainly, due to compliance problems, the age below 3 years may be reasonably considered a practical contraindication. Conclusions: Given that some specific AIT products are effective and approved as drugs (AIFA, EMA, FDA), the use in children is still debated. Some aspects still need robust confirm: (a) the safety of AIT in asthma; (b) the optimal regimen of administration; (c) the role of AIT as preventative treatment for asthma development. [ABSTRACT FROM AUTHOR]

Asthma and influenza are two pathologic conditions of the respiratory tract that affect millions worldwide. Influenza virus of the 2009 pandemic was highly transmissible and caused severe respiratory disease in young and middle-aged individuals. Asthma was discovered to be an underlying co-morbidity that led to hospitalizations during this influenza pandemic albeit with less severe outcomes. However, animal studies that investigated the relationship between allergic inflammation and pandemic (p)H1N1 infection, showed that while characteristics of allergic airways disease were exacerbated by this virus, governing immune responses that cause exacerbations may actually protect the host from severe outcomes associated with influenza. To better understand the relationship between asthma and severe influenza during the last pandemic, we conducted a systematic literature review of reports on hospitalized patients with asthma as a co-morbid condition during the pH1N1 season. Herein, we report that numerous other underlying conditions, such as cardiovascular, neurologic, and metabolic diseases may have been underplayed as major drivers of severe influenza during the 2009 pandemic. This review synopses, (1) asthma and influenza independently, (2) epidemiologic data surrounding asthma during the 2009 influenza pandemic, and (3) recent advances in our understanding of allergic host-pathogen interactions in the context of allergic airways disease and influenza in mouse models. Our goal is to showcase possible immunological benefits of allergic airways inflammation as countermeasures for influenza virus infections as a learning tool to discover novel pathways that can enhance our ability to hinder influenza virus replication and host pathology induced thereof.

Purpose: The objective of this study was to examine patient characteristics, treatment patterns, and exacerbations among patients with asthma newly treated with omalizumab., Methods: Data for this study were obtained from administrative claims and medical records. The index date was the date of the first claim for omalizumab. All patients had ≥12 months of continuous health plan eligibility before and after the index date. Demographic and clinical characteristics were obtained 12 months before the index date. Treatment patterns of asthma medications, including omalizumab, and asthma exacerbations were evaluated in the preindex and postindex periods., Findings: The study included 1564 patients. Asthma-related medication use decreased from the preindex to the postindex periods (oral corticosteroids, 83.3%-66.4%, P < 0.001; inhaled corticosteroids [ICSs], 33.1%-26.8%, P < 0.001; long-acting β 2 -adrenergic agonists [LABAs], 6.6%-5.2%, P = 0.009; ICS-LABA combination, 69.3%-64.3%, P < 0.001; leukotriene modifiers, 67.8%-59.7%, P < 0.001). The proportion of patients with any asthma exacerbations decreased by 33.6% (66.6%-44.2%, P < 0.001). Notably, the relative decreases in hospitalization and emergency department exacerbations were 79.3% and 72.2%, respectively. A total of 930 patients (59.5%) discontinued omalizumab treatment during the entire postindex period (maximum, 3400 days [approximately 9 years]), with 353 (38.0%) restarting omalizumab treatment., Implications: In this real-world analysis, patients newly initiating omalizumab therapy for allergic asthma used fewer concomitant asthma medications, while experiencing significant reductions in asthma exacerbations, especially hospitalization- and emergency department-specific exacerbations, from pre- to post-omalizumab treatment initiation periods., (Copyright © 2018 Elsevier Inc. All rights reserved.)

It has been 50 years since the dust mite was first appreciated to be a major source of allergen in house dust, and by extension a key trigger of allergic respiratory disease. Since that time a number of protein allergens have been identified and characterized, mainly from mite feces, and standardized mite extracts and IgE assays have been developed. Insights into the lifecycle of dust mites and aspects of mite allergen biology have shed light on the mechanisms that lead to respiratory disease and to the development of interventions that can minimize dust mite allergen exposure. It is now clear that dust mite allergy is a key contributor to asthma in many parts of the world, and that long-term avoidance can be effective for preventing sensitization and minimizing the development and severity of respiratory disease. Here, we discuss the evidence linking dust mites with respiratory disease, outline studies that support the efficacy of home environmental interventions, and highlight practical methods that have been shown to be effective as part of a multifaceted approach to dust mite avoidance., (Copyright © 2017 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Subcutaneous immunotherapy and sublingual immunotherapy are effective for allergic rhinitis and allergic asthma and with some support for use in selected patients with atopic dermatitis. The sequence of immunologic responses is the same, irrespective of the route of administration, and similar disease modification has been demonstrated. However, there are differences between the two approaches. The most important is the greatly reduced likelihood of sublingual immunotherapy producing systemic reactions. There are major drawbacks for sublingual immunotherapy in regard to dosing. Finally, there is the question of relative clinical efficacy, with the currently available data favoring subcutaneous immunotherapy., (Copyright © 2016 Elsevier Inc. All rights reserved.)