AllergyPub Date : 2025-07-29DOI: 10.1111/all.16681
Pedro Botelho Alves,Carmela Pablo-Torres,Aspasia Karavelia,Ruben Fernandez-Santamaria,Mattia Giovannini,Leticia de Las Vecillas,Mohammed Shamji,Maria Jose Torres
{"title":"Addressing the Growing Role of Junior Members in EAACI.","authors":"Pedro Botelho Alves,Carmela Pablo-Torres,Aspasia Karavelia,Ruben Fernandez-Santamaria,Mattia Giovannini,Leticia de Las Vecillas,Mohammed Shamji,Maria Jose Torres","doi":"10.1111/all.16681","DOIUrl":"https://doi.org/10.1111/all.16681","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"31 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Efficacy of ASA Therapy After Desensitization on CRSwNP Patients With Asthma and N-ERD-A Randomized Clinical Trial.","authors":"Alma Helevä,Annina Lyly,Viljami Salmi,Mika Mäkelä,Paula Kauppi,Anu Laulajainen-Hongisto,Lena Hafrén,Paula Virkkula,Mikko Nuutinen,Sanna Toppila-Salmi","doi":"10.1111/all.16679","DOIUrl":"https://doi.org/10.1111/all.16679","url":null,"abstract":"Non-steroidal anti-inflammatory drug (NSAID) exacerbated respiratory disease (N-ERD) is a chronic inflammatory condition typically involving hypersensitivity to NSAIDs, asthma, and/or chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP). N-ERD increases the risk for severe hypersensitivity reactions, recurring sinonasal surgeries, or the need for systemic corticosteroid treatment. Aspirin (ASA) treatment after desensitization (ATAD) is a treatment option for N-ERD. Desensitization to ASA is reached with increasing ASA doses over a few days, followed by a long-term treatment. This study evaluated the efficacy of ATAD with an ASA dose of 250 mg in adult CRSwNP patients with asthma and N-ERD. Forty-one CRSwNP patients with comorbid asthma and N-ERD were recruited for this randomized double-blind clinical trial. Twenty-six patients had successful ASA desensitization, were randomized into placebo and ASA arms, and continued to 11 months of daily ASA, with a target dose of 250 mg. The outcome measures, including Sino-Nasal Outcome Test 22 (SNOT-22), nasal polyp score (NPS), Asthma Control Test (ACT), and EPOS 2012 CRS clinical control assessment, were evaluated at control visits at 1, 5, 11, and 12 months after the start of the treatment. In the linear mixed effects model, p-values for the combined effect of group and time showed no difference between placebo and ATAD for SNOT-22, ACT, and NPS, with p-values 0.17, 0.45, and 0.18, respectively. Neither group showed significant improvement in the EPOS 2012 CRS control assessment. In conclusion, no significant clinical difference was observed between ATAD and placebo in the treatment of CRSwNP patients with asthma and N-ERD.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"24 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AllergyPub Date : 2025-07-29DOI: 10.1111/all.16682
Anish Dsilva, Ariel Wagner, Michal Itan, Natalie Rhone, Shmulik Avlas, Yaara Gordon, Natalie Davidian, Shraddha Sharma, Elizaveta Razravina, Israel Zan-Bar, Jane R Parnes, Kevin S Gorski, Joseph D Sherrill, Chen Varol, Steven F Ziegler, Marc E Rothenberg, Ariel Munitz
{"title":"Distinct Roles for Thymic Stromal Lymphopoietin (TSLP) and IL-33 in Experimental Eosinophilic Esophagitis.","authors":"Anish Dsilva, Ariel Wagner, Michal Itan, Natalie Rhone, Shmulik Avlas, Yaara Gordon, Natalie Davidian, Shraddha Sharma, Elizaveta Razravina, Israel Zan-Bar, Jane R Parnes, Kevin S Gorski, Joseph D Sherrill, Chen Varol, Steven F Ziegler, Marc E Rothenberg, Ariel Munitz","doi":"10.1111/all.16682","DOIUrl":"10.1111/all.16682","url":null,"abstract":"<p><strong>Rationale: </strong>Thymic stromal lymphopoietin (TSLP) and IL-33 are alarmins implicated in eosinophilic esophagitis (EoE) pathogenesis by activating multiple cells, including mast cells (MCs). Whether TSLP or IL-33 have a role in EoE and whether their activities are distinct requires further investigation.</p><p><strong>Methods: </strong>Experimental EoE was induced in wild type (WT) Il33<sup>-/-</sup> and Crlf2<sup>-/-</sup> mice. TSLP or IL-5 were neutralized using antibodies. Esophageal histopathology was determined by H&E, anti-Ki67, anti-CD31, and anti-MBP staining. Esophageal RNA was subjected to RNA sequencing. Bone marrow-derived MCs were activated with TSLP and IL-13 was determined (ELISA).</p><p><strong>Results: </strong>TSLP and IL-33 were overexpressed in human and experimental EoE. Human and mouse esophageal MCs displayed the highest level of Crlf2 (TSLPR) compared to other immune cells. Crlf2<sup>-/-</sup> mice were nearly completely protected from EoE, and TSLP neutralization resulted in decreased basal cell proliferation, eosinophilia, lamina propria thickening, and vascularization. Induction of experimental EoE in Il33<sup>-/-</sup> mice resulted in reduced eosinophilia, but no alterations in tissue remodeling were observed compared to WT mice. RNA sequencing revealed that TSLP regulates the expression of key genes associated with human EoE (e.g., eotaxins, Il19, Klk5, Flg, Il36rn, Il1r2) and suggests a role for TSLP in regulating IL-1 signaling, barrier integrity, and epithelial cell differentiation. Experimental EoE was characterized by a MC-associated gene signature and elevated MCs. Activation of MCs with TSLP resulted in the secretion of IL-13.</p><p><strong>Conclusion: </strong>TSLP and IL-33 have non-redundant functions in experimental EoE. This study highlights TSLP as an upstream regulator of IL-13 and a potential therapeutic target for EoE.</p>","PeriodicalId":122,"journal":{"name":"Allergy","volume":" ","pages":""},"PeriodicalIF":12.0,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ficolin-A Protects Against Allergic Asthma via Suppressing ILC2-Drived Type 2 Inflammation.","authors":"Yu-Ke Xie,Shan-Shan Xu,Yong-Shuai Li,Jiarong Li,Shu-Chen Zhang,Yan Xie,Ya-Dong Gao,Xiao-Lian Zhang","doi":"10.1111/all.16661","DOIUrl":"https://doi.org/10.1111/all.16661","url":null,"abstract":"BACKGROUNDType 2 inflammation has emerged as a pivotal mechanism for asthma, which involves both innate and adaptive immunity. Human ficolin (FCN)-2 (L-ficolin, P35) and its mouse homolog FCN-A are one of the major pattern recognition molecules of plasma/serum, acting as important initiators of the lectin complement system and playing important roles in immunity, including respiratory immunity. However, little is known about the role of FCN-2/A in allergic asthma.METHODSSerum FCN-2 and IgE levels in 90 allergic asthmatic patients and 48 healthy controls were measured by ELISA. Aeroallergen house dust mite (HDM)-induced mouse model of asthma was generated in both wild type (WT) and FCN-A knockout (KO) mice. Mouse serum and bronchoalveolar lavage fluid (BALF) IgE levels, lung innate lymphoid cells (ILC)1/2/3, the expression of transcription factors GATA3, T-bet, and RORγt, and the concentrations of type 2 cytokines in serum and BALF were measured by FCM, RT-qPCR, Western blot, and ELISA.RESULTSSerum FCN-2 concentrations in patients with allergic asthma were significantly lower than those in healthy controls. Similarly, lower serum and BALF FCN-A concentrations were observed in HDM-induced asthma mouse models compared to those of uninduced mice. In the asthma mouse model, FCN-A KO asthmatic mice had higher levels of total IgE and HDM-specific IgE (sIgE), β-hexosaminidase (β-HEX) and histamine secretion, as well as increased airway epithelial permeability with the release of FITC-dextran in sera, inflammatory cell infiltration and eosinophil counts, and displayed more severe disease symptoms with histological damage compared to WT asthmatic mice. FCN-A KO asthmatic mice showed decreased T-bet+ ILC1 and increased IL-5+/IL-13+ ILC2/ILC2 proportions, p-GATA3 expression, serum and BALF type 2 cytokines IL-4, IL-5, and IL-13, Th17 cytokine IL-17, and chemokines CCL2/4 production. Importantly, the administration of exogenous FCN-A protected against mouse allergic airway inflammation with decreased ILC2 proportions and type 2 cytokines expression, serum total and allergen-specific IgE production. These results suggest that FCN-A suppresses both ILC2 innate immunity and IgE-mediated adaptive immunity during asthma.CONCLUSIONOur findings provide previously unreported evidence that FCN-A protects against allergic asthma by suppressing lung ILC2-driven type 2 inflammation.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"98 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AllergyPub Date : 2025-07-24DOI: 10.1111/all.16663
Gabriele Cortellini,Alla Nakonechna,Annick Barbaud,Sevim Bavbek,Gianfranco Calogiuri,Inmaculada Doña,Violeta Kvedariene,Jose Julio Laguna Martinez,Serena Liberati,Mauro Pagani,Antonino Romano
{"title":"Diagnosis and Management of Hypersensitivity to Antiplatelet Drugs: EAACI Position Paper.","authors":"Gabriele Cortellini,Alla Nakonechna,Annick Barbaud,Sevim Bavbek,Gianfranco Calogiuri,Inmaculada Doña,Violeta Kvedariene,Jose Julio Laguna Martinez,Serena Liberati,Mauro Pagani,Antonino Romano","doi":"10.1111/all.16663","DOIUrl":"https://doi.org/10.1111/all.16663","url":null,"abstract":"Antiplatelet drug (APD) therapy is the cornerstone for the prevention of atherosclerotic cardiovascular disease. The main APDs are aspirin and thienopyridines, particularly clopidogrel. These drugs may induce hypersensitivity reactions (HSRs). The most common reported reactions to these drugs are cutaneous, such as exanthemas associated with thienopyridine and urticaria/angioedema by aspirin, which can also induce respiratory symptoms. APDs other than aspirin, particularly ticlopidine, can also cause hematologic reactions consisting mainly of isolated thrombocytopenia, agranulocytosis, and leukopenia. Immune-mediated reactions to aspirin are very rare. Few data suggest the usefulness of skin testing in patients with cutaneous reactions to APDs other than aspirin, particularly clopidogrel. Therefore, the drug provocation test is the gold standard for diagnosing hypersensitivity to APDs. Low-dose aspirin challenge (i.e., up to 150-180 mg) and aspirin desensitization have emerged as effective and safe approaches in patients with suspected or confirmed aspirin hypersensitivity who require aspirin therapy. Both, a short course of oral glucocorticoids without interruption of clopidogrel treatment and desensitization, appears to be effective and safe options in patients with cutaneous HSRs to clopidogrel. This position paper provides data and recommendations regarding the characteristics of HSRs to APDs and related diagnostic procedures in order to make them as safe and effective as possible. Management and treatment options, including desensitization protocols, are also provided.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"11 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144693203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AllergyPub Date : 2025-07-22DOI: 10.1111/all.16627
Aleix Arnau‐Soler, Sarah E. Ashley, Ahla Ghauri, Alexander C. S. N. Jeanrenaud, Ingo Marenholz, Katharina Blumchen, Penelope Cibin, Alisa Iakupova, Norbert Hubner, Kirsten Beyer, Young‐Ae Lee
{"title":"Understanding the Variability of Peanut‐Oral Immunotherapy Responses by Multi‐Omics Profiling of Immune Cells","authors":"Aleix Arnau‐Soler, Sarah E. Ashley, Ahla Ghauri, Alexander C. S. N. Jeanrenaud, Ingo Marenholz, Katharina Blumchen, Penelope Cibin, Alisa Iakupova, Norbert Hubner, Kirsten Beyer, Young‐Ae Lee","doi":"10.1111/all.16627","DOIUrl":"https://doi.org/10.1111/all.16627","url":null,"abstract":"BackgroundOral immunotherapy (OIT) induces desensitization in peanut allergy, yet 15%–30% of patients do not respond, and a significant risk of anaphylaxis due to treatment remains. In a placebo‐controlled peanut OIT trial, this study identifies molecular drivers of OIT responsiveness through multi‐omics profiling in immune cells.MethodsImmunoglobulins, cytokines, transcriptome, and DNA methylome profiles were analyzed in peanut‐stimulated and unstimulated peripheral blood mononuclear cells isolated from peanut‐allergic children before and after treatment. Multi‐omics profiling focused on OIT responsiveness within the active treatment arm. Additional subgroup analyses were performed to further elucidate molecular mechanisms and potential biomarkers.ResultsComplete responders, tolerating 4500 mg of peanut protein, exhibited lower pre‐treatment peanut‐specific IgE and Th2 cytokine production (IL‐4, IL‐5) compared to incomplete responders who tolerated ≤ 1000 mg of peanut protein after treatment. Our primary analysis identified 184 differentially expressed genes and 1001 differentially methylated genes, enriched for innate (ILC3) and adaptive (CD8αα subset of CD8<jats:sup>+</jats:sup> T cells) immune cells, alongside γδ T cells and exosomes, highlighting gastrointestinal regulatory processes as central to OIT success. We found a marked downregulation of immunoglobulin genes in patients receiving peanut compared to placebo, suggesting OIT‐induced modulation of B‐cell activity. Functional networks revealed a marked imbalance contrasting regulatory T‐cell responses and B‐cell suppression in the complete responders with innate immune signaling and metabolic stress in the incomplete responders.ConclusionThis multi‐omics approach underscores the importance of gastrointestinal immune mechanisms underlying the variation in peanut oral immunotherapy responses and offers potential biomarkers for improving treatment strategies.Trial RegistrationGerman Clinical Trials Register DRKS00004553","PeriodicalId":122,"journal":{"name":"Allergy","volume":"17 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144678014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epithelial Lining Fluid Cystatin SN is a Noninvasive Biomarker for Predicting Type 2 Chronic Rhinosinusitis.","authors":"Seojin Moon,Sungmin Moon,Sol Lee,Gyeongyeob Kim,Min-Seok Koo,Hyung-Ju Cho,Chang-Hoon Kim,Min-Seok Rha","doi":"10.1111/all.16652","DOIUrl":"https://doi.org/10.1111/all.16652","url":null,"abstract":"BACKGROUNDAs treatment responses differ according to the inflammatory endotype of chronic rhinosinusitis (CRS), identifying the endotype could facilitate personalized treatment. We aimed to identify a noninvasive epithelial lining fluid (ELF) biomarker for the type 2 (T2) endotype of CRS.METHODSNasal tissue and ELF samples were obtained from patients with CRS and control individuals. Single-cell RNA sequencing (scRNA-seq) data were analyzed. The expression of inflammatory mediators was measured using Luminex multiplex assays and enzyme-linked immunosorbent assays.RESULTSAnalysis of the scRNA-seq data revealed that CST1 was exclusively expressed in epithelial cells of T2 CRS, but not in those of non-T2 CRS, and this was confirmed by immunofluorescence staining. Cystatin SN expression was detected in ELF, and its levels were significantly higher in T2 CRS than in non-T2 CRS and controls. The expression level of cystatin SN in the ELF was positively correlated with the Lund-Mackay CT, SNOT-22, and JESREC scores, whereas it was inversely correlated with olfactory function. Furthermore, ELF cystatin SN levels correlated with the tissue/blood eosinophil count and nasal tissue expression of T2 inflammatory mediators, indicating that ELF cystatin SN is a reliable marker of nasal T2 inflammation. In the receiver operating characteristics curve analysis evaluating the predictive efficacy for T2 CRS, the AUC for ELF cystatin SN was 0.894 (0.936 in the validation cohort), which was higher than that of other markers, including blood eosinophil count, serum total IgE level, and the JESREC score. With a cut-off value of 112.5 ng/mg, ELF cystatin SN yielded a 75.0% sensitivity and 92.0% specificity.CONCLUSIONSELF cystatin SN is a clinically feasible, noninvasive biomarker with superior accuracy for predicting T2 CRS.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"15 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sugar Intake and Respiratory Consequences: Deciphering the Link Between Drink Choice and Asthma Risk.","authors":"Fasty Arum Utami,Nam Nhat Nguyen,Shih-Yi Huang,Shiu-Wen Huang,Chih-Ming Weng,Yang-Ching Chen","doi":"10.1111/all.16667","DOIUrl":"https://doi.org/10.1111/all.16667","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"12 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144664199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AllergyPub Date : 2025-07-19DOI: 10.1111/all.16647
Mohamed F Jeebhay,Hille Suojalehto,Susan M Tarlo,Eva Suarthana,Paul Cullinan,Irmeli Lindström,Paola Mason,Xavier Munoz,Monika Raulf,Marcela Valverde,Jolanta Walusiak-Skorupa,Paul Henneberger
{"title":"A Novel Questionnaire and Algorithm for Work-Related Asthma Screening and Surveillance: An EAACI Task Force Report.","authors":"Mohamed F Jeebhay,Hille Suojalehto,Susan M Tarlo,Eva Suarthana,Paul Cullinan,Irmeli Lindström,Paola Mason,Xavier Munoz,Monika Raulf,Marcela Valverde,Jolanta Walusiak-Skorupa,Paul Henneberger","doi":"10.1111/all.16647","DOIUrl":"https://doi.org/10.1111/all.16647","url":null,"abstract":"INTRODUCTIONWork-related exposures contribute to one in six new-onset adult asthma cases and exacerbation of one in five existing cases, which together are termed 'work-related asthma' (WRA). A valid and standardized WRA questionnaire is needed for workplace surveillance and epidemiological studies. This project aimed to review evidence on WRA questionnaires and algorithms to propose a standardized instrument.METHODSA scoping review was conducted using PubMed, Embase, and Cochrane databases up to March 2021. Search terms focused on asthma, occupational diseases, questionnaires, surveys, and algorithms. High-quality studies were identified and data extracted on instrument construction, validation, and performance. Common questions were used to develop a questionnaire and algorithm for detecting suspected WRA.RESULTSSix studies were included. The final WRA questionnaire consists of eight questions on general asthma symptoms, diagnosis, and medication; four on WRA symptoms; and two on work-related ocular-nasal symptoms. The algorithm calculates a WRA total score (WRATS) based on the general asthma and work-related symptoms. A score of ≥ 1 triggers a referral for further evaluation.CONCLUSIONThis is the first WRA questionnaire based on validated questionnaires. Evaluation of its performance and validation in diverse geographic and occupational settings are needed for further refinement and translation for broader applications.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"8 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144664198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}