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        <title>Frontiers in Allergy | Asthma section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/allergy/sections/asthma</link>
        <description>RSS Feed for Asthma section in the Frontiers in Allergy journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-13T21:23:23.368+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1666241</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1666241</link>
        <title><![CDATA[Actual use of PROMs in asthma and rhinitis recommended by guidelines in clinical settings: PROMUSE respiratory study]]></title>
        <pubdate>2026-04-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ivan Cherrez-Ojeda</author><author>Jean Bousquet</author><author>Torsten Zuberbier</author><author>Juan C. Calderon</author><author>Pavel Kolkhir</author><author>Anastasiia Allenova</author><author>Andrey Allenov</author><author>Sergey Tkachenko</author><author>Florin Mihaltan</author><author>Ruxandra Ulmeanu</author><author>Mona Al-Ahmad</author><author>Mònica Rodriguez-González</author><author>Guillermo Wakida-Kusunoki</author><author>German D. Ramon</author><author>Maia Rukhadze</author><author>Désirée E. Larenas-Linnemann</author><author>Mitja Košnik</author><author>Juan Carlos Ivancevich</author><author>Luis Felipe Ensina</author><author>Nelson A. Rosario Filho</author><author>Violeta Kvedariene</author><author>Herberto Jose Chong-Neto</author><author>Ivan Tinoco</author><author>Anna Bedbrook</author><author>Gabriela Rodas-Valero</author><author>Marco Faytong-Haro</author><author>Marcus Maurer</author><author>Oliver Pfaar</author><author>Karla Robles-Velasco</author>
        <description><![CDATA[RationaleGuidelines advise for the implementation of patient-reported outcomes (PROMs) to provide crucial insights into patients' perceptions of their disease burden, treatment needs, and quality of life. Despite their proven benefits in managing chronic respiratory diseases like asthma, allergic rhinitis (AR), and rhinosinusitis (RS), there is limited data on their adoption among physicians treating these conditions.ObjectivesOur objective is to identify the utilization patterns of PROMs, together with the reasons for their usage and the barriers to their adoption among practitioners managing patients with asthma, AR, and RS.MethodsThis was a cross-sectional observational study using a questionnaire encompassing all pertinent PROMs and disseminated to practitioners associated with the ARIA, UCARE, ADCARE, and ACARE networks. Individuals unfamiliar with PROMS or lacking prior experience with it were eliminated. Descriptive and analytical data were utilized, categorized by the frequency and type of PROMs applied. Stata 18.0 was utilized, with p < 0.05 indicating statistical significance.ResultsA total of 439 practitioners participated, with PROMs predominantly utilized by physicians certified for over 30 years and by respiratory specialists (16.67% and 12.46%, respectively; p < 0.05). Pulmonologists exhibited the greatest utilization of asthma PROMs at 86%, while allergists predominantly employed AR and RS PROMs at 38.42% and 33.33%, respectively (p < 0.001). ACT (66.74%), RCAT (27.79%), and SNOTT22 (15.26%) were the predominant PROMs utilized primarily for asthma (79.19%), AR (51.23%), and RS (57.26%), respectively (p < 0.001). The foremost purposes for their application were disease control monitoring (93.39%) and evaluation of performance of therapy approaches (90.2%). The most significant barrier identified was time constraint, rated at 75.40% (p > 0.05 across all groups).ConclusionsThe use of PROMs is suboptimal, primarily due to time limitations. It is imperative that methods be swiftly implemented to include these techniques into the therapeutic environment to attain enhanced outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1740307</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1740307</link>
        <title><![CDATA[The testosterone paradox in asthma]]></title>
        <pubdate>2026-04-23T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Ynuk Bossé</author>
        <description><![CDATA[Asthma and an excessive response to inhaled methacholine, commonly called hyperresponsiveness, are intimately linked. Therefore, factors increasing the methacholine response are expected to contribute to asthma as well. However, this is clearly not the case for testosterone, the predominant sex hormone in males. While testosterone increases the methacholine response, it is rather protective in asthma and experimental asthma. These incompatible observations are referred herein as the ‘testosterone paradox’, and the chase is now on to unravel its underlying mechanisms.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1772380</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1772380</link>
        <title><![CDATA[Asthma and corticosteroids “odi et amo”: how to deal with it?]]></title>
        <pubdate>2026-04-13T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Luca Borsari</author><author>Laura Carbonieri</author><author>Luca M. Verdini</author><author>Valentina Ruggieri</author><author>Bianca Beghe’</author>
        <description><![CDATA[Asthma is a chronic, heterogeneous respiratory disease that affects more than 300 million individuals worldwide and is responsible for substantial morbidity, mortality and healthcare burden. Chronic airway inflammation plays a central role in symptom expression, disease progression, and response to therapy. Corticosteroids, both inhaled and systemic, are the cornerstone of asthma treatment. However, it is well known that the use and abuse of systemic corticosteroids is almost invariably associated to the development of significant acute and chronic adverse events. Epidemiological data report that despite the availability of new target therapy, e.g., biologics, in real practice systemic steroids are still overused, and in this review, we highlight strategies 1) to identify and screen patients at risk of developing corticosteroids adverse events and 2) to reduce them.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1840104</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1840104</link>
        <title><![CDATA[Editorial: Biologics for airway diseases: from bench to bedside]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Andreas M. Matthaiou</author><author>Nikoleta Bizymi</author><author>Dina Visca</author><author>Lena Uller</author><author>Nikolaos G. Papadopoulos</author><author>Alexander G. Mathioudakis</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1667661</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1667661</link>
        <title><![CDATA[One-session asthma curriculum for all K–8th grade students: impact on knowledge, attitudes, and self-efficacy]]></title>
        <pubdate>2026-04-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Caroline Luff</author><author>Alexandra Knitter</author><author>Bolanle Ogbara</author><author>LaToya Gregory</author><author>Monica Kowalczyk</author><author>Anna Volerman</author>
        <description><![CDATA[BackgroundSchools are critical places to support children with asthma. Few school-based interventions focus on classmates without asthma, who can influence peers’ asthma self-management.ObjectiveTo describe a one-session asthma curriculum for all Kindergarten-8th grade students and evaluate impact on knowledge, attitudes, and self-efficacy.MethodsIn collaboration with three Chicago schools, we adapted and implemented a one-session asthma curriculum for K-8th grades. Students completed a post-session survey to assess asthma knowledge, attitudes, and self-efficacy. Pearson's Chi-squared tests analyzed differences between grades and student-reported asthma diagnosis.ResultsIn total, 603 students participated in a session, of which 485 completed the survey; 19% reported having asthma. Most students correctly answered knowledge questions on pathophysiology (82%), transmission (79%), symptoms (65%), triggers (65%), medication use (90%), and episode management (51%). More older students understood pathophysiology (85% vs. 72%, p = 0.002), medication use (93% vs. 83%, p = 0.002), and episode management (55% vs. 31%, p < 0.001), vs. younger students. Of all students, 83% indicated positive attitudes about asthma care and 49% about physical activity participation, with differences based on grade (asthma care: older 86% vs. younger 74%, p = 0.002) and diagnosis (physical activity participation: asthma 63% vs. no asthma 45%, p = 0.002). Most students indicated positive self-efficacy to help classmates with asthma episodes (74%), with more younger students doing so than older students (83% vs. 71%, p = 0.01).ConclusionStudents had high asthma knowledge and self-efficacy after a one-session all-student asthma curriculum; attitudes were mixed. School-based asthma education is feasible and has positive outcomes for all K–8th grade students.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1789783</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1789783</link>
        <title><![CDATA[Impact of sputum neutrophilia on the efficacy of biologics in severe asthma]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Patrizia Pignatti</author><author>Martina Zappa</author><author>Francesco Ardesi</author><author>Marco Vanetti</author><author>Rosella Centis</author><author>Antonio Spanevello</author><author>Dina Visca</author>
        <description><![CDATA[IntroductionPatients with severe asthma have new therapeutic opportunities with biologic agents, reducing exacerbation rates, symptom scores, and oral corticosteroid use; however, their effects on lung function appear to be variable. The aim of this study is to evaluate the clinical and inflammatory outcomes of biologic therapy in patients with severe asthma, stratified according to baseline bronchial inflammation.MethodsThis was a retrospective observational study in patients with severe asthma at 6 and 12 months after initiation of biologic therapy. Patients were categorized according to their baseline airway inflammatory profile. The inflammatory biomarkers evaluated included induced sputum, fractional exhaled nitric oxide (FeNO), and peripheral blood leukocyte counts. Lung function, comorbidities, exacerbation rate, and asthma control (assessed by ACQ-6 and ACT) were also recorded.ResultsA total of 113 patients with severe asthma were analyzed. Patients with a paucigranulocytic pattern were excluded from further analyses due to their small number (n = 10). Among the remaining subjects (n = 103), 62.8% exhibited an eosinophilic pattern, 13.3% a mixed granulocytic pattern, and 15.0% a neutrophilic pattern. Most neutrophilic patients (82.7%) presented elevated type 2 (T2) biomarkers (FeNO and/or blood eosinophils). Differences in baseline biomarkers and comorbidities reflected the underlying airway inflammatory patterns; forced vital capacity (FVC, L) was lower in neutrophilic patients compared with the other groups. Neutrophilic patients had higher frequencies of obstructive sleep apnea and lower chronic rhinosinusitis with nasal polyps than eosinophilic subjects. During follow-up, all patients showed a significant reduction in their ability to produce sputum (p < 0.001), as well as significant decreases in exacerbation rate and symptom burden. Eosinophilic and mixed granulocytic patients exhibited significant improvements in lung function, whereas neutrophilic patients did not. Only eosinophilic patients showed a significant reduction in airway inflammation. Oral corticosteroid doses decreased across all groups, but significantly only in eosinophilic patients. Clinical and inflammatory improvements were observed after 6 months of biologic therapy, with no further significant changes at 12 months.ConclusionsAfter 12 months of biologic therapy, patients showed phenotype-dependent responses, with neutrophilic patients demonstrating smaller clinical and inflammatory improvements compared with those with eosinophilic or mixed granulocytic phenotypes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1766647</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1766647</link>
        <title><![CDATA[Depemokimab demonstrates efficacy in patients with type 2 asthma with comorbid CRSwNP: Phase III SWIFT-1/-2 analysis]]></title>
        <pubdate>2026-03-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Enrico Heffler</author><author>Diana Jarreta</author><author>Chang-Qing Zhu</author><author>Anna Vichiendilokkul</author><author>Peter Howarth</author><author>Anju Peters</author><author>Santiago Quirce</author><author>David J. Jackson</author>
        <description><![CDATA[IntroductionThe efficacy of twice-yearly depemokimab was demonstrated in the Phase III SWIFT-1/-2 trials for type 2 asthma characterized by blood eosinophils, and ANCHOR-1/-2 trials for chronic rhinosinusitis with nasal polyps (CRSwNP). Up to 40% of patients with severe asthma are estimated to have comorbid CRSwNP, an overlap associated with increased disease burden. Depemokimab may therefore offer meaningful clinical benefit in this subpopulation. This analysis evaluated the efficacy of depemokimab in patients with type 2 asthma and comorbid CRSwNP using pooled data from SWIFT-1/-2.MethodsPatients with type 2 asthma were randomized 2:1 to receive depemokimab 100 mg subcutaneously or placebo, plus standard of care, every 26 weeks for 52 weeks. Pre-specified outcomes included annualized exacerbation rates over 52 weeks, and St George's Respiratory Questionnaire (SGRQ) and Asthma Control Questionnaire-5 (ACQ-5) scores over 52 weeks, analyzed by baseline comorbid CRSwNP subgroup.ResultsIn the asthma with CRSwNP subgroup, the annualized rate of exacerbations over 52 weeks was lower in patients who received depemokimab [0.51 (95% CI: 0.34, 0.75); n = 80] vs. placebo [1.61 (95% CI: 0.99, 2.60); n = 33], with a rate ratio (95% CI) of 0.31 (0.17, 0.58). Additionally, an improvement in least squares (LS) mean SGRQ total score in the depemokimab group vs. placebo was noted after 4 weeks of treatment [−7.12-point difference (95% CI: −13.41, −0.83)] which was sustained up to 52 weeks [−8.32-point difference (95% CI: −15.77, −0.88)] in the asthma with CRSwNP subgroup. Similarly, an improvement from baseline in LS mean ACQ-5 score was noted with depemokimab vs. placebo after 2 weeks of treatment [−0.40-point difference (95% CI: −0.79, −0.01)], which was maintained up to 52 weeks [−0.76-point difference at (95% CI: −1.23, −0.28)] in the asthma with CRSwNP subgroup.DiscussionTwice-yearly depemokimab reduced annualized exacerbation rates and demonstrated greater improvements in SGRQ and ACQ-5 scores vs. placebo in patients with type 2 asthma and comorbid CRSwNP. These improvements were greater than those reported in the overall SWIFT-1/-2 population. These findings identify that type 2 asthma with CRSwNP is a clinically recognizable phenotype that is likely to have enhanced benefit with depemokimab therapy.Clinical trial identifiersNCT04719832/NCT04718103.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1746439</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1746439</link>
        <title><![CDATA[Long-term Qipian® administration confers resistance to airway inflammation in OVA-induced asthmatic mice]]></title>
        <pubdate>2026-02-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Huiying Wang</author><author>Ru-Yi Chen</author><author>Jin-Jin Shi</author><author>Guan-Jun Yang</author><author>Jiong Chen</author>
        <description><![CDATA[BackgroundQipian® is an immunomodulatory agent with established short-term benefits in allergic asthma, but its long-term effects remain unclear. This study aimed to investigate its potential to attenuate the development of asthma in a murine model and to elucidate its underlying mechanisms.MethodsMice received oral Qipian® for 3 months prior to establishment of an ovalbumin (OVA)-induced asthma model. Samples (lung tissues, blood, bronchoalveolar lavage fluid, and feces) were collected. Analyses included quantification of eosinophils, immunoglobulins, and Th1/Th2 cytokines. Lung mucus was assessed via periodic acid-Schiff staining; dendritic cell and regulatory T (Treg) cell populations were characterized by flow cytometry; and gut microbiota was profiled via 16S rDNA sequencing. Asthmatic symptoms were scored concurrently.ResultsLong-term Qipian® administration (LTQA) effectively reduced OVA-induced asthmatic symptoms, airway inflammation, inflammatory cell infiltration, and mucus hypersecretion. LTQA restored the Th1/Th2 balance by reducing IL-4, IL-5, and IL-13, while elevating the expression of IFNγ and IL-10. Furthermore, LTQA was associated with the expansion of Tregs and CD103+ dendritic cells, reduction of OVA-elevated neurokinins [neurokinin A (NKA), neurokinin B (NKB)], and increased abundance of Lactobacillus.ConclusionThis study indicates that LTQA may confer resistance to allergic airway inflammation by modulating immune responses and gut microbiota supporting the lung–gut axis as a promising target for novel clinical approaches in asthma management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1738118</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1738118</link>
        <title><![CDATA[Understanding disease burden, challenges in current treatment strategies and call for action for management of severe asthma in Asia: a position statement from Asian respiratory experts]]></title>
        <pubdate>2026-02-26T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Mariko Siyue Koh</author><author>Ken Ka Pang Chan</author><author>Koichi Fukunaga</author><author>Sang-Heon Kim</author><author>Le Thi Tuyet Lan</author><author>Azza Omar</author><author>Thitiwat Sriprasart</author><author>Deepak Talwar</author><author>Min Zhang</author><author>Shih-Lung Cheng</author>
        <description><![CDATA[In the Asia-Pacific region, there is limited data on the full extent of the burden of severe asthma, as well as a lack of clear guidance on improving care standards. Genetic, environmental, behavioural, policy and funding factors in -Asia-Pacific region differ from other parts of the world. To address these gaps, a panel of Asian experts conducted a comprehensive review of the existing literature in the region, aiming to understand the burden of severe asthma and provide key recommendations and actionable steps to improve its management across Asia. Experts identified several key challenges in managing SA, which include inadequate expertise, delayed patient identification or referral, limited access to advanced diagnostics and treatments, suboptimal adherence, and insufficient government support and funding, underlining the need for a more comprehensive approach to SA management. Experts also proposed that the Asia-Pacific region definition of clinical remission in SA should include elimination of exacerbation and use of oral corticosteroids, good symptom control, and inclusion of lung function criteria, particularly in light of the evolving treatment landscape. The experts concluded that while restoring normal lung function may be unrealistic for most patients with severe asthma and remodelled airways, striving for optimal individual lung function or maintaining stability may be a more attainable goal. Several key points and actionable recommendations were proposed to help reduce the overall burden of severe asthma in Asia.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1797785</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1797785</link>
        <title><![CDATA[Editorial: The role of epithelial-derived cytokines in airway disease]]></title>
        <pubdate>2026-02-24T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Hector Ortega</author><author>Kian Fan Chung</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1758940</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1758940</link>
        <title><![CDATA[Silent invaders: the role of MPs on epithelium inflammation and damage in airway diseases]]></title>
        <pubdate>2026-02-16T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Benedetta Bondi</author><author>Stefania Nicola</author><author>Federico Di Marco</author><author>Sara Chiappori</author><author>Luisa Brussino</author><author>Laura De Ferrari</author><author>Anna Maria Riccio</author><author>Fulvio Braido</author><author>Diego Bagnasco</author>
        <description><![CDATA[Microplastics (MPs) and Nanoplastics (NPs) have emerged as pervasive environmental contaminants with growing implications for respiratory health. Increasing evidence demonstrates that inhaled MPs can deposit throughout the airways, interact with epithelial surfaces, and trigger a cascade of inflammatory, oxidative, and structural alterations that may contribute to the onset or progression of airway diseases. Their pathogenicity is influenced by physicochemical properties, including size, shape, density, and surface charge, which determine their aerodynamic behavior, epithelial penetration, and cellular uptake. Once deposited, MPs are associated with epithelial stress responses, including oxidative stress, activation of inflammatory signaling pathways, and alterations in junction-related proteins, which may impair mucociliary function. Smaller particles and NPs are internalized through endocytosis, leading to mitochondrial dysfunction, reactive oxygen species (ROS) generation, and activation of key inflammatory pathways such as NF-κB, PI3K/Akt/mTOR, and Wnt/β-catenin. These mechanisms promote cytokine release, epithelial–mesenchymal transition, and dysregulated repair responses. Experimental and clinical evidence indicate that MPs exacerbate epithelial fragility in asthma and COPD by amplifying oxidative stress, enhancing barrier dysfunction, and intensifying maladaptive crosstalk between epithelial and immune cells. In fibrotic pathways, persistent epithelial injury activates the NLRP3 inflammasome and drives TGF-β1-mediated fibroblast activation and extracellular matrix deposition, establishing a self-perpetuating cycle of inflammation and remodeling. Emerging data suggest a potential role for MPs in lung carcinogenesis through chronic inflammation, indirect genotoxic effects mediated by oxidative stress, and altered cellular homeostasis. Overall, MPs represent an underrecognized but increasingly relevant environmental factor capable of inducing epithelial damage, promoting chronic airway inflammation, and contributing to the pathophysiology of asthma, COPD, pulmonary fibrosis, and possibly lung cancer. Understanding these mechanisms is crucial to guide preventive strategies, regulatory policies, and future clinical research. This review critically evaluates current experimental evidence on microplastic–epithelium interactions, highlighting mechanistic insights, methodological limitations, and key gaps that must be addressed to clarify their role in airway diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1741154</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1741154</link>
        <title><![CDATA[Association between impulse oscillometry Z-scores and asthma control and exacerbation risk in a tertiary severe asthma clinic]]></title>
        <pubdate>2026-02-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Li Ping Chung</author><author>Dylan Beinart</author><author>Emily S. Y. Goh</author><author>Gregory G. King</author>
        <description><![CDATA[IntroductionRespiratory oscillometry is a sensitive tool for assessing small airways dysfunction. However, limited evidence on cutoff values for interpretation remains a barrier to its clinical use. The aim of this study was to determine whether the presence and severity of abnormalities, defined by Z-scores for oscillometric parameters, are associated with asthma symptoms and exacerbation risk.MethodsWe retrospectively reviewed the medical records of all patients with asthma managed in a severe asthma clinic between 2019 and 2022 who underwent routine oscillometry. Z-scores for oscillometric parameters were analyzed as continuous and categorical variables to assess their associations with asthma control and exacerbation risk.ResultsWhen analyzed as categorical variables, Z-score-defined severity thresholds for resistance (R5), reactance (X5), and the area under the reactance curve (AX) were associated with levels of asthma control (as measured by the ACQ5). When analyzed as continuous variables, Z-scores were also correlated with worst asthma control (as assessed by both ACQ5 and the asthma control test) (P < 0.005). These correlations remained significant after adjustment for spirometric indices, FeNO, and treatment changes. Elevated Z-scores (>1.64) for R5 were associated with a higher risk of exacerbations (OR 2.70, 95% CI 1.27–5.17, P = 0.009). The risk of exacerbation increased with the severity of airway obstruction. Similar trends were observed for AX and X5; however, these associations did not reach statistical significance.DiscussionThe presence and severity of airway obstruction, as defined by R5 Z-scores, predict poorer asthma control and an increased risk of exacerbations. Similar associations with asthma control were also observed for X5 and AX Z-scores. Clinicians should use Z-scores over other cutoffs to aid interpretation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1748679</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1748679</link>
        <title><![CDATA[EGFR inhibitors suppress house dust mite allergen Der pII induced inflammation in monocytes and macrophages]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ya-Hui Chiang</author><author>I-Lun Hsin</author><author>Ping-Ju Chen</author><author>Hui-Yi Chang</author><author>Jiunn-Liang Ko</author><author>Ko-Huang Lue</author><author>Yu-Fan Liu</author>
        <description><![CDATA[IntroductionAllergic asthma, often triggered by house dust mites (HDMs), is characterized by airway inflammation, mucus hypersecretion, and airway hyperresponsiveness. Among the major HDM allergens, Der pII plays a significant role in promoting inflammation. This study investigates the role of epidermal growth factor receptor (EGFR) inhibitors in modulating Der pII-induced cytokine production and inflammation in human immune cells.MethodsRecombinant GST-Der pII protein was expressed and purified for subsequent studies. Human peripheral blood mononuclear cells (HPBMC), THP-1 monocytes, THP-1-derived macrophages, and pulmonary alveolar macrophages (NR8383) were exposed to Der pII, followed by treatment with EGFR inhibitors AZD-9291 and Tarceva. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expressions of IL-6 and IL-8. Nitric oxide (NO) levels were determined using the Griess Reagent System.ResultsDer pII significantly induced pro-inflammatory cytokines, including IL-6, IL-8, and TNF-α in HPBMC and THP-1 cells. Both EGFR inhibitors reduced the secretion of IL-6 and IL-8 in these cell types. In THP-1 macrophages, AZD-9291 suppressed IL-6 expression and CD14/CD36 macrophage markers. Moreover, AZD-9291 significantly inhibited NO production in alveolar macrophages.ConclusionsThese findings suggest that EGFR plays a critical role in mediating Der pII-induced inflammation, and EGFR inhibitors may represent a potential therapeutic approach for controlling HDM-induced allergic inflammation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1731295</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1731295</link>
        <title><![CDATA[Pentraxin 3 deficiency exacerbates neutrophilic inflammation and airway hyperresponsiveness in type 2-low asthma]]></title>
        <pubdate>2026-02-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sina Taefehshokr</author><author>Lianyu Shan</author><author>Mojdeh Matloubi</author><author>Sujata Basu</author><author>A. Halayko</author><author>Abdelilah S. Gounni</author>
        <description><![CDATA[BackgroundType 2-low asthma is a severe, steroid-resistant phenotype characterized by neutrophilic inflammation and limited treatment options. PTX3, an acute-phase protein involved in innate immunity, has been linked to inflammatory diseases; but its role in type 2-low asthma remains unclear.MethodsA chronic HDM + c-di-GMP murine model was used to mimic type 2-low asthma. PTX3−/− and WT mice were assessed for inflammation, cytokine profiles, antibody responses, and lung function. AHR was measured using FlexiVent. BALF inflammatory cells were analyzed by cytospin and flow cytometry. Cytokines were quantified using mesoscale assay, and serum immunoglobulins by ELISA.ResultsIn mice, the type 2-low model exhibited increased systemic and airway PTX3 levels. PTX3−/− mice exposed to the type 2-low protocol developed significantly greater airway inflammation, with higher total BALF cell counts and a 2-fold increase in neutrophils, but no change in eosinophils. PTX3 deficiency led to increased total and HDM-specific IgE levels. BALF cytokine analysis revealed elevated IL-17A in PTX3−/− mice, while IL-4, IL-5, and IL-13 remained unchanged. PTX3−/− mice also exhibited significantly higher AHR parameters.ConclusionsPTX3 absence enhances neutrophilic inflammation, IL-17A production, IgE responses, and AHR, highlighting PTX3 as a potential biomarker and therapeutic target in type 2- low asthma.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2025.1707834</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2025.1707834</link>
        <title><![CDATA[A randomized, double-blind, placebo-controlled trial of soluble corn fiber supplementation for children with asthma]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Clinical Trial</category>
        <author>Matthew A. Rank</author><author>Daisy L. Barroso</author><author>Kathryn A. Conn</author><author>Melissa Pecak</author><author>Matthew Scandura</author><author>Allyson H. Hirsch</author><author>Haiwei Gu</author><author>Corrie M. Whisner</author><author>Heather Shearer</author><author>Darcy Johnson</author><author>Natalia Argel</author><author>Cindy S. Bauer</author><author>Sophia N. Williams</author><author>Benjamin L. Wright</author><author>James Woodward</author><author>Emily K. Cope</author>
        <description><![CDATA[IntroductionAsthma is a multifactorial disease influenced by genetic and environmental factors, including diet. The gut microbiome contributes to airway inflammation via the gut-lung axis, partly through production of short chain fatty acids (SCFAs) from bacterial fermentation of dietary fiber. We hypothesized that dietary fiber supplementation could modulate the gut microbiome and increase SCFAs in children with asthma.MethodsThis is a double-blind, placebo-controlled trial of children who were randomized to consume 12 g of soluble corn fiber (SCF) as a supplement to their usual daily diet (50% the recommended daily fiber intake) or placebo for 4–6 weeks (clinicaltrials.gov NCT03673618). Dietary surveys, asthma symptom questionnaires, fecal, blood and nasal samples were collected before and after the intervention period to quantify fiber intake, asthma control, nasal and gut microbiome, and serum short chain fatty acids (SCFAs).ResultsOf the 20 children enrolled, 15 completed the intervention with an average adherence rate of 83%. SCFA concentrations and gut microbiome changes varied by individual and treatment group. No significant differences in gut or nasal alpha or beta diversity were observed between groups post-intervention. However, differential abundance analysis showed a trend toward increased Bifidobacterium in the SCF group compared to placebo (ANCOM-BC p = 0.0004, FDR q = 0.073).DiscussionSupplementation of 50% of recommended daily fiber intake had minimal impact on asthma symptoms, the microbiome, or SCFA levels. Future studies should consider higher fiber doses, different fiber types, or targeting individuals with low baseline fiber intake to account for observed variability in microbiome and SCFA responses.Clinical Trial Registrationhttps://clinicaltrials.gov/study/NCT03673618, identifier NCT03673618.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2025.1759789</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2025.1759789</link>
        <title><![CDATA[Editorial: Exploring the interconnection: obesity's role in asthma development and management]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Akira Yamasaki</author><author>Katsuyuki Tomita</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2025.1635540</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2025.1635540</link>
        <title><![CDATA[Case Report: Extending dosing intervals of biologics in adults severe asthma: a case series]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Tomoya Harada</author><author>Miyu Nishigami</author><author>Hiroyuki Tanaka</author><author>Genki Inui</author><author>Hiroki Ishikawa</author><author>Hiroki Kohno</author><author>Yoshihiro Funaki</author><author>Tomohiro Sakamoto</author><author>Miki Takata</author><author>Ryota Okazaki</author><author>Masato Morita</author><author>Shin Kitatani</author><author>Akira Yamasaki</author>
        <description><![CDATA[BackgroundBiological therapies have improved the control of severe asthma. However, biological therapies are expensive. Therefore, the cost-effective use of these medications after achieving improved disease control warrants consideration.MethodsThis retrospective case series analyzed 69 adult patients with asthma who received biological therapies at our department between 2009 and 2023. Among them, 11 patients underwent dosing interval extension. We collected data on their clinical characteristics, asthma control status, and changes in clinical parameters after interval extension.ResultsAt the time of dosing interval extension, the mean patient age was 62.1 years, with 5 female patients. Omalizumab was used in five cases, benralizumab in five, and dupilumab in one. The dosing intervals were extended by 1.5 to 2 times. The median duration from the initiation of biologics to interval extension was 7.0 months, with 6 patients undergoing extension within the first 7 months. One year after extension, asthma exacerbation occurred in only one patient receiving omalizumab. The frequency of exacerbations and the proportion of patients receiving oral corticosteroids (OCS) were decreased. The median ACT score remained at 25, while the median daily OCS dose decreased from 5.0 mg to 4.0 mg (prednisolone equivalent). The median % predicted FEV₁ changed from 84.9% to 78.3%.ConclusionsFor patients whose asthma control improves after initiating biological therapy, extending the dosing interval may be a feasible treatment option. Given the retrospective, single-center design and small sample size, these findings are exploratory and generate hypotheses that require validation in larger, prospective studies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1757445</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1757445</link>
        <title><![CDATA[Biologic therapies for severe pediatric asthma: efficacy, safety, and biomarker-guided selection]]></title>
        <pubdate>2026-01-20T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Enrico Tondina</author><author>Alessia Claudia Codazzi</author><author>Riccardo Castorina</author><author>Rossana Di Micco</author><author>Cristina Dutto</author><author>Livia Leoncini Bartoli</author><author>Giovanni Lepore</author><author>Gian Luigi Marseglia</author><author>Ilaria Brambilla</author>
        <description><![CDATA[BackgroundSevere pediatric asthma is a heterogeneous, high-burden disease marked by variable corticosteroid responsiveness, frequent exacerbations, and substantial impairment in quality of life. Advances in airway immunobiology, particularly the delineation of type-2 (T2) pathways (IgE, IL-5, IL-4/IL-13) and epithelial alarmins, have enabled the development of targeted biologic therapies for biomarker-defined patient subgroups.ObjectiveTo synthesize current evidence on the efficacy and safety of biologic therapies for severe pediatric asthma and to translate biomarker-driven selection into practical clinical guidance, while outlining emerging therapeutic directions.Summary of findingsTargeted biologics, anti-IgE (omalizumab), anti-IL-5/IL-5Rα (mepolizumab, benralizumab; pediatric data for reslizumab remain limited), anti-IL-4Rα (dupilumab), and anti-TSLP (tezepelumab) improve disease control, reduce severe exacerbations, and enable steroid-sparing in appropriately selected children. Benefits are greatest in T2-high profiles, particularly with elevated blood eosinophils and/or fractional exhaled nitric oxide (FeNO), while tezepelumab shows efficacy across biomarker strata. Lung-function gains are modest to moderate but clinically meaningful. Persisting gaps include optimal treatment duration, stopping rules, long-term safety, cost, and equitable access.ConclusionsBiologic therapies have reshaped the care of severe pediatric asthma, operationalizing precision medicine through immunologic endotyping and biomarker-guided selection. Priorities now include standardized definitions of response and remission, robust long-term safety data, and strategies to ensure equitable access across diverse pediatric populations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2025.1754173</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2025.1754173</link>
        <title><![CDATA[Endotype-driven decisions in choosing a biologic for airway diseases]]></title>
        <pubdate>2026-01-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Carmen Panaitescu</author><author>Laura Haidar</author><author>Maria-Roxana Buzan</author><author>Răzvan-Ionuț Zimbru</author><author>Valentin-Cristian Iovin</author><author>Elena-Larisa Zimbru</author><author>Alexandru Lăculiceanu</author><author>Ioana Agache</author>
        <description><![CDATA[The increasing availability of biologic therapies for allergic diseases has highlighted the need for more precise, mechanism-based patient selection. Traditional approaches based on disease phenotypes often fall short in predicting therapeutic response. Escalating healthcare costs together with questions about the efficacy of the current management of allergic diseases prompt to a shift toward endotype-driven and biomarker-guided strategies. This review explores the role of endotypes, defined by distinct immunologic, molecular, or cellular mechanisms, in guiding the use of targeted biologics in asthma and in chronic rhinosinusitis with nasal polyps. Endotype classification based on the type 1, type 2 and type 3 immune response is critical for selecting biologics targeting the IgE, IL-5, IL-4/IL-13, or TSLP pathways. The endotype-driven approach in allergic diseases has tremendous potential if incorporated into comprehensive care pathways, with endotype identification playing a key role in the management decision tree, with improved outcomes and greater patient satisfaction. To this purpose this review provides decision algorithms for the endotype-guided approach at the point of care and discusses the unmet needs with potential practical solutions to support a personalized precision approach.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2025.1719820</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2025.1719820</link>
        <title><![CDATA[Using biomarkers and independent predictors of therapy response to optimize treatment of uncontrolled severe asthma in the biologic era]]></title>
        <pubdate>2026-01-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Hideki Yasui</author>
        <description><![CDATA[Severe asthma is a chronic respiratory disease characterized by a lack of control with maximal standard therapy or exacerbation upon therapy reduction. Recent advances in the diagnosis and management of severe asthma have improved patient outcomes. An improved mechanistic understanding of asthma has revealed that many cases are driven by type 2 inflammation, which can be targeted with biologic agents including omalizumab (anti-IgE), mepolizumab and reslizumab (anti-IL-5), benralizumab (anti-IL-5Rα), dupilumab (anti-IL-4Rα), and tezepelumab (anti-thymic stromal lymphopoietin). Biomarkers, including elevated fractional exhaled nitric oxide, blood eosinophil counts, and serum IgE levels, have been validated for the diagnosis of severe asthma and can be used to help guide disease management. These biologic agents and biomarkers have changed the clinical management of severe asthma, making it possible to pursue the goal of clinical remission. However, despite these advances, a proportion of patients continue to experience uncontrolled severe asthma, which has significant implications for disease management and quality of life. In this review, I briefly examine the current state of biologics and biomarkers in the treatment of uncontrolled severe asthma, and draw on my clinical experience to highlight limitations to optimal management, including persistent treatment heterogeneity. After discussing emerging biomarkers and predictors of disease status and treatment response, I provide my perspective on future approaches and research directions that may enhance clinical treatment and improve patient outcomes.]]></description>
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