Allergy最新文献

{"title":"Pathways of Epithelial Barrier Breakdown and Remodeling in Esophageal Organoids by Commonly Used Surfactants","authors":"Ozge Ardicli, Duygu Yazici, Huseyn Babayev, Yagiz Pat, Manal Bel Imam, Hang Du, Hassan Melhem, Carina Beha, Laura Buergi, Anja Heider, Juan-Felipe López, Sena Ardicli, Can Zeyneloğlu, Andrea Kreienbühl, Nino Stocker, Patrick Westermann, Christoph B. Messner, Mübeccel Akdis, Jan Hendrik Niess, Alain Schoepfer, Luc Biedermann, Cezmi A. Akdis, Swiss EoE Cohort Study Group, Willem van de Veen","doi":"10.1111/all.70490","DOIUrl":"10.1111/all.70490","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Eosinophilic esophagitis (EoE) is a chronic immune-mediated disease characterized by symptoms of esophageal dysfunction, such as dysphagia and food impaction, as well as eosinophilic inflammation and impaired epithelial barrier integrity, which promotes allergen influx. Environmental exposures that weaken the esophageal barrier, including surfactants found in personal care products such as sodium dodecyl sulfate (SDS) and cocamidopropyl betaine (CAPB), have been proposed as contributors to disease susceptibility. However, their direct effects on esophageal epithelial barrier function and associated molecular responses remain insufficiently characterized.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We investigated the molecular and functional consequences of SDS and CAPB exposure in primary EoE-derived esophageal organoids and air-liquid interface cultures derived from biopsy tissue samples. We conducted transepithelial electrical resistance (TEER) measurements, paracellular flux assays, RNA sequencing, targeted and untargeted proteomics, and immunofluorescence imaging.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Treatment of esophageal organoids with SDS or CAPB (0–100 μg/mL) caused dose-dependent cytotoxicity and barrier disruption, with SDS producing stronger effects. At 12.5 μg/mL, viability declined to ~30% with SDS versus ~60% with CAPB, accompanied by greater TEER reduction and ~2-fold higher permeability. RNA-seq of organoids exposed to 12.5 μg/mL for 24 h showed distinct transcriptomic clustering, with 2749 shared and > 1500 surfactant-specific differentially expressed genes, indicating broad epithelial remodeling, cell-cycle suppression, and stress responses, more pronounced under SDS. SDS preferentially activated inflammatory and innate immune pathways, which was supported by proteomic detection of elevated cytokines (TNF, IL-8, IL-18, etc.). Both surfactants induced keratinization, epidermal cell differentiation, and partial epithelial-mesenchymal transition signatures, including increased vimentin without E-cadherin loss.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings demonstrate that common surfactants can induce coordinated epithelial stress responses in esophageal tissue models and may act as environmental aggravating factors in EoE at relatively low doses. This work underscores the need to consider mucosal exposure to consumer product ingredients in the context of epithelial barrier disorders, particularly surfactants such as SDS and CAPB, and supports efforts to refine","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3659-3672"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.70490","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148823482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nasal Epithelial Immune Signatures Are Associated With Age-Dependent Asthma Trajectories in Early Life","authors":"Constanze A. Jakwerth,&nbsp;Sabina Illi,&nbsp;Helen Charles,&nbsp;Madlen Oelsner,&nbsp;Amr A. Gabr,&nbsp;Ulrich M. Zissler,&nbsp;Anna Erb,&nbsp;Martin Feuerherd,&nbsp;Felix Drost,&nbsp;Maren Büttner,&nbsp;Benjamin Schubert,&nbsp;Nicole Maison,&nbsp;Jimmy Omony,&nbsp;Markus Weckmann,&nbsp;Ruth Grychtol,&nbsp;Anna-Maria Dittrich,&nbsp;Svenja Foth,&nbsp;Chrysanthi Skevaki,&nbsp;Tobias Trojan,&nbsp;Silke van Koningsbruggen-Rietschel,&nbsp;Gesine Hansen,&nbsp;Thomas Bahmer,&nbsp;Klaus F. Rabe,&nbsp;Folke Brinkmann,&nbsp;Matthias Volkmar Kopp,&nbsp;Ulrike Protzer,&nbsp;Adam M. Chaker,&nbsp;Bianca Schaub,&nbsp;Erika von Mutius,&nbsp;Carsten B. Schmidt-Weber,&nbsp;the ALLIANCE Study Group as part of the German Center for Lung Research (DZL)","doi":"10.1111/all.70477","DOIUrl":"10.1111/all.70477","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Preschool wheeze is heterogeneous and only a subset of children progresses to persistent asthma. We hypothesized that early-life wheeze reflects divergent airway epithelial maturation trajectories associated with distinct mucosal immune programs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Nasal epithelial transcriptomes from 265 children and young adults (79 healthy, 81 wheezers, 105 asthmatics; median age 10.4 [1.1–20.3] years) from the All Age Asthma Cohort (ALLIANCE) cohort were analyzed using a hypothesis-driven candidate approach based on predefined cytokine axes. Transcriptional signatures were mapped to epithelial cells by scRNA-sequencing. Asthma-outcome associations were assessed in age- and sensitization-adjusted multivariate models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The candidate approach identified three antagonistic epithelial immune programs: an interferon-associated (E1; IDO1, CSF3, CCL20), a type-2-associated (E2; POSTN, CCL26, CST1), and a type-17-associated program (E3; IL36G, KLK7, KRTDAP). These programs were detected across basal, ciliated, and secretory epithelial cells. In early childhood (1–3 years), wheezers predominantly exhibited E1/E3-dominant epithelial profiles (<i>n</i> = 36). Age-group-specific comparisons showed higher E2 and lower E1/E3 expression in wheezers aged 4–6 years (<i>n</i> = 38) than in those aged 1–3 years (<i>n</i> = 36). E2 dominance correlated with IgE, FeNO, and eosinophilia (<i>p</i> &lt; 0.01). In multivariate models assessing asthma outcome at age 6, E1 expression was inversely associated with asthma persistence (OR = 0.15, <i>p</i> &lt; 0.05), whereas E3 expression was associated with disease progression (OR = 4.93, <i>p</i> &lt; 0.05). The combined epithelial signature discriminated asthma outcomes with high accuracy (AUC = 0.90), independent of allergic sensitization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Early-life wheeze reflects distinct airway epithelial immune programs characterized by age-associated patterns in epithelial immune activity. Nasal epithelial transcriptional signatures capture molecular trajectories associated with asthma persistence and may enable early risk stratification.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>All-Age-Asthma (ALLIANCE) cohort: clinicaltrials.gov: NCT02496468; adult arm: NCT02419274</p>\u0000 </section>\u0000 </div>","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3533-3553"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.70477","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148899725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultra-Processed Food Consumption and Childhood Allergic Diseases: Increased Risk of Asthma Onset in the SENDO Project","authors":"O. Galindo,&nbsp;M. J. Goikoetxea,&nbsp;L. Moreno-Galarraga,&nbsp;L. Argiz,&nbsp;J. M. Moreno-Villares,&nbsp;Victor de la O,&nbsp;N. Martín-Calvo","doi":"10.1111/all.70378","DOIUrl":"10.1111/all.70378","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>While the role of genetic predisposition in asthma and other allergic conditions is well established, the contribution of nutritional patterns is heterogeneous and has been demonstrated in cross-sectional studies but not in prospective cohorts.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed data from 1546 participants enrolled in the SENDO cohort between January 2015 and June 2024. Children aged 4–5 years were prospectively recruited. UPF consumption was assessed at baseline and updated at the 3-year follow-up. Information on asthma and allergic diseases was collected at baseline and updated annually during the follow-up. A final sample of 691 participants was classified into tertiles (T1, T2, T3) according to UPF consumption. Prevalent cases were excluded from the analysis to ensure that incident cases were included during the follow-up. In the main analyses, we calculated the adjusted hazard ratios (HRs) and 95% CI with survival analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After a mean follow-up of 3.4 years, the adjusted risk for asthma in each tertile (T1, T2, T3) of UPF consumption was 2.6%, 9.9%, and 7.6% respectively (p for trend: 0.03). In the fully adjusted model of the survival analysis, children with greater UPF consumption (T2 + T3) showed a significantly higher risk of asthma (HR 3.76; 95% CI 1.15–11.51, <i>p</i> = 0.02) but not of AA, nor other allergic outcomes compared with their peers in the lowest tertile (T1) of UPF consumption.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Higher UPF consumption may be associated with an increased risk of developing asthma in school-age children.</p>\u0000 </section>\u0000 </div>","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3504-3514"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.70378","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147831189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal Follow-Up of Gut and Salivary Microbiota in Children With Food Protein-Induced Enterocolitis Syndrome","authors":"Anais Lemoine,&nbsp;Karine Adel-Patient,&nbsp;Nathalie Kapel,&nbsp;Camille Mayeur,&nbsp;Marie-Noelle Rossignol,&nbsp;Aurelia Bruneau,&nbsp;Patrick Tounian,&nbsp;Muriel Thomas,&nbsp;Ioannis Nicolis","doi":"10.1111/all.70363","DOIUrl":"10.1111/all.70363","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Gut microbiota and their metabolites play a key role in digestive dysimmunity and tolerance breakdown, leading to pathologies such as food protein-induced enterocolitis syndrome (FPIES). This study aimed to compare both the gut and salivary microbiota over time between the allergic and tolerant patients and the matched controls.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Faecal and salivary samples were collected longitudinally from FPIES allergic patients on an elimination diet, and after their natural tolerance acquisition, and from matched controls (1:1 ratio). 16S rRNA gene sequencing and biostatistical analyses (ALDEx2, ANCOM-BC, DESeq2, LEfSe, and MaAsLIN2) were used to compare microbiota composition between groups. The measurement of faecal short-chain fatty acids (SCFAs) using gas chromatography evaluated the gut microbiota functions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Thirty-eight allergic patients were included (median age: 1.3 years), and 22 became tolerant over time. Allergic patients exhibited lower gut and salivary alpha-diversities, and several different genera (12 in stools, including less <i>Ruminococcus</i>, and 2 in saliva), and higher relative abundance of acetate than the controls. With tolerance acquisition, faecal alpha-diversities partially increased, whereas SCFAs normalised. Ultimately, there were more differences in faecal and salivary microbiota in allergic patients versus after tolerance acquisition (i.e., more <i>Blautia</i>, <i>Ruminococcus</i>, <i>Faecalibacterium</i>, <i>Prevotella</i>-9, and less <i>Escherichia</i>–<i>Shigella</i> in tolerant patients) than between the controls over time.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The faecal and salivary dysbiosis observed in allergic patients with FPIES partially resolved after tolerance acquisition. Understanding the underlying mechanisms of dysbiosis is crucial to prevent and help manage FPIES. A prolonged follow-up could determine whether dysbiosis resolution may be complete, and whether this early infancy dysbiosis has long-term consequences on health.</p>\u0000 </section>\u0000 </div>","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3608-3619"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.70363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147754891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Common Food Emulsifiers Impair Epithelial Barrier Integrity and Trigger Pro-Inflammatory Responses and IgE Production","authors":"Duygu Yazici,&nbsp;Yuka Hayashi,&nbsp;Yagiz Pat,&nbsp;Jennifer Hotie,&nbsp;Mehmet Ali Balci,&nbsp;Sena Ardicli,&nbsp;Juan Felipe Lopez,&nbsp;Ozge Ardicli,&nbsp;Bingjie Zhao,&nbsp;Angel Maldonado,&nbsp;Can Zeyneloglu,&nbsp;Kenji Matsumoto,&nbsp;Manru Li,&nbsp;Beate Rückhert,&nbsp;Lihong Chang,&nbsp;Ismail Ogulur,&nbsp;Vahap Eldem,&nbsp;Raja Dhir,&nbsp;Mubeccel Akdis,&nbsp;Kari Nadeau,&nbsp;Oscar Palomares,&nbsp;Hideaki Morita,&nbsp;Cezmi A. Akdis","doi":"10.1111/all.70473","DOIUrl":"10.1111/all.70473","url":null,"abstract":"<p>The global rise in allergic and autoimmune diseases since the 1960s has been associated with environmental disruptions of epithelial barriers, particularly in the gastrointestinal tract. Among the implicated factors are food emulsifiers, which have become increasingly prevalent in processed foods such as peanut butter. This study investigates the biological effects of two commonly used food emulsifiers in peanut butter, soy lecithin and diacetyl tartaric acid esters of mono- and diglycerides (DATEM), on gastrointestinal tissue responses and immune responses using advanced in vitro gut-on-a-chip models, human adult stem cell-derived colon organoids-on-a-chip, and murine models. Both emulsifiers induced dose-dependent cytotoxicity and disrupted epithelial barriers, as demonstrated by reduced transepithelial electrical resistance and disorganization of zona occludens-1 at daily-exposure doses. Transcriptomic and proteomic analyses revealed activation of pro-inflammatory pathways including TNF, NF-κB, the unfolded protein response, and cell death by apoptosis. Soy lecithin additionally induced oxidative stress. Systemic responses were confirmed by increased pro-inflammatory cytokines in serum and immune activation in peripheral blood mononuclear cells (PBMCs). Notably, both emulsifiers stimulated serum total IgG, soy lecithin induced IgE in mice upon feeding, and DATEM enhanced IL-4-induced IgE production in human PBMCs, suggesting a role in allergy development. These findings challenge the presumed safety of soy lecithin and DATEM and highlight their potential contribution to immune dysregulation and epithelial barrier dysfunction, which may initiate or exacerbate food allergy and gastrointestinal inflammatory diseases.</p>","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3641-3658"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.70473","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148687858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated CO2 and Temperature Alter Grass Pollen's Ability to Modify Transcriptome and Function of the Nasal Epithelium","authors":"Tarleena Tossavainen,&nbsp;Tanja Turunen,&nbsp;Maria-Viola Martikainen,&nbsp;Miisa Kankaanpää,&nbsp;Marjo Malinen,&nbsp;Marjut Roponen","doi":"10.1111/all.70251","DOIUrl":"10.1111/all.70251","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Climate change increases exposure to pollen, but the effects of climate-related factors on the potency of pollen to trigger early events in the epithelium are unknown, despite their significant impact on respiratory health.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We aimed to investigate whether climate change affects the capacity of grass pollen to mediate cell functions in human nasal epithelium.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Toxicological and immunological responses, and the transcriptomes were analyzed after exposing reconstituted human nasal epithelial tissues to pollen collected from grasses (timothy and meadow foxtail) grown under different climate change conditions (increasing temperature and CO₂ levels).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Pollen of both grass species grown under current climate conditions altered the expression of genes encoding for cytokines and chemokines, and similar patterns were observed at the protein level. Moreover, pollen exposure reduced epithelial barrier integrity and was associated with increased expression of genes related to tight junctions and tissue repair. Climate change-modified meadow foxtail pollen decreased the expression of genes related to vesicle-mediated transport and transcriptional and translational processes, whereas pollen of timothy grass inhibited the expression of genes related to cilium assembly and organization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Future grass pollen potentially disrupts cilia function and vesicle-mediated (cytokine) signaling in human nasal epithelium more than pollen representing current climate. That may hinder appropriate immune reaction activation and foreign substance removal from the airways. Disrupted regulation of gene expression in turn potentially results in adverse system-level outcomes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3554-3567"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.70251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146153529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detergent-Containing Toothpaste Decreases Esophageal Mucosal Impedance and Alters Salivary Properties in Humans","authors":"Benjamin L. Wright,&nbsp;Michael D. Crowell,&nbsp;Huijun Luo,&nbsp;Mia Y. Masuda,&nbsp;Naohiro Itoh,&nbsp;Karalyn Folmes,&nbsp;Jean M. Stoa,&nbsp;Matthew R. Buras,&nbsp;Will Sherman,&nbsp;Saurabh Baheti,&nbsp;Dean Bowman,&nbsp;Lindsey C. Hill,&nbsp;Marcelo F. Vela,&nbsp;Hirohito Kita,&nbsp;Matthew A. Rank,&nbsp;David B. Hill,&nbsp;Jennifer L. Horsley-Silva,&nbsp;Alfred D. Doyle","doi":"10.1111/all.70437","DOIUrl":"10.1111/all.70437","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Eosinophilic esophagitis is associated with epithelial barrier dysfunction. Epidemiologic studies suggest environmental factors promote disease pathogenesis. The common household detergent sodium dodecyl sulfate (SDS) induces epithelial barrier dysfunction and eosinophilic inflammation in mice. We hypothesized that acute SDS exposure would compromise the esophageal mucosal barrier in humans.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Healthy adults brushed with 2 g of an SDS-containing toothpaste. Esophageal impedance was measured continuously pre-/post-toothbrushing to assess the effect of toothpaste on epithelial barrier function. SDS was measured in saliva using a methylene blue anionic substances assay. Participants completed 1-h esophageal string tests (ESTs) pre-/post-toothbrushing and protein isolates from EST eluates from the proximal and distal esophagus were analyzed by tandem mass tag mass spectrometry.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ten of twelve subjects completed the clinical study. SDS in the initial expectorate measured immediately after toothbrushing varied markedly (median: 321.40 μg/mL; range: 169.90–1243.00 μg/mL) and was detectable in saliva in 80% of subjects (median: 9.55 μg/mL; range: 0–123.40 μg/mL) at 60 min post toothbrushing. Esophageal mucosal impedance decreased within 30 min of toothbrushing (<i>p</i> &lt; 0.01). Toothbrushing increased salivary viscosity and proteins associated with mucosal defense in EST eluates. The tight junction pathway was downregulated while the salivary secretion and complement and coagulation cascades pathways were upregulated in the proximal esophagus.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In healthy individuals, SDS remained detectable in saliva for a prolonged period after toothbrushing at concentrations previously shown to disrupt esophageal epithelial barrier function in vitro. Toothbrushing with an SDS-containing toothpaste was associated with reduced esophageal mucosal impedance, altered salivary properties, and activated mucosal immune responses.</p>\u0000 </section>\u0000 </div>","PeriodicalId":122,"journal":{"name":"Allergy","volume":"81 10","pages":"3631-3640"},"PeriodicalIF":11.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148371981","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":"Exploring the Link Between Environmental Exposures and Disease via Direct Challenge.","authors":"Anna M Erickson, Ian A Myles, Jodi L Blake, Cezmi A Akdis, Hirsh D Komarow","doi":"10.1111/all.70537","DOIUrl":"10.1111/all.70537","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":" ","pages":""},"PeriodicalIF":11.3,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126220","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":"Algorithms in Allergy: Treatment of Hypereosinophilic Syndromes, 2026 Update","authors":"Guillaume Lefèvre, Florence Roufosse, Giacomo Emmi, Andreas Reiter, Emmanuel Ledoult, Jean‐Emmanuel Kahn","doi":"10.1111/all.70533","DOIUrl":"https://doi.org/10.1111/all.70533","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"1 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149086979","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":"Selective Absence of Co‐Inhibitory Receptor‐Expressing CD4 + T Cells in Lungs of Obese House Dust Mite‐Allergic C57BL /6 Mice","authors":"Sarah Miethe, Daniel P. Potaczek, Kim Pauck, Andrea Berlin, Bilal Alashkar Alhamwe, Stefanie Hagner, Andrea Nist, Elke Pogge von Strandmann, Thorsten Stiewe, Paul Klemm, Hartmann Raifer, Clemens Thölken, Holger Garn","doi":"10.1111/all.70492","DOIUrl":"https://doi.org/10.1111/all.70492","url":null,"abstract":"Background Asthma and obesity are highly prevalent chronic inflammatory diseases, the mutual pathomechanistic relationships of which have not been fully elucidated yet. We hypothesized that inflammatory mechanisms in obese adipose tissue influence the phenotype of an induced allergic airway inflammation (AAI) with altered activation processes in CD4 <jats:sup>+</jats:sup> T cells being involved in this interaction. Methods C57BL/6 and BALB/c mice were fed high‐fat (HFD) or normal (ND) diet for several weeks and subjected to a house dust mite (HDM)‐induced model of AAI mimicking main features of human asthma. Inflammatory and metabolic parameters were assessed and lung CD45 <jats:sup>+</jats:sup> cells were deep‐phenotyped using flow cytometry and targeted single cell CITE‐Seq (cellular indexing of transcriptomes and epitopes by sequencing) analysis. Results Despite comparable metabolic changes in both strains in response to HFD, only C57BL/6 mice developed excessive weight gain. In both strains, the chosen HDM exposure protocol induced a mixed AAI phenotype characterized by eosinophil and neutrophil airway infiltration in ND‐fed mice. However, only in C57BL/6 mice, concomitant HFD resulted in changed eosinophils to neutrophils ratios and a higher proportion of lung CD4 <jats:sup>+</jats:sup> T cells. Using single‐cell CITE‐Seq, a specific subcluster of CD4 <jats:sup>+</jats:sup> T cells was identified exclusively in the lungs of lean, but not in obese, HDM‐exposed C57BL/6 mice, characterized by the expression of co‐inhibitory receptors such as CTLA‐4, PD‐1, and LAG‐3. Furthermore, culturing pre‐differentiated T cells in the presence of supernatants from hypertrophic adipocytes resulted in reduced frequencies of cells expressing these receptors. Conclusion The presence of co‐inhibitory receptor‐expressing CD4 <jats:sup>+</jats:sup> T cells in lean mice with AAI may represent a disease‐limiting mechanism, which is abolished by a co‐existing obesity resulting in intensified inflammatory processes in the lungs. This mechanism could explain higher asthma severity observed in obese patients.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"50 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149086734","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}