Rakesh Natarajan, Brooke Szczesny, Kanika Kanchan, Erika Esquinca, Meher Preethi Boorgula, Sameer Chavan, Monica Campbell, Wendy Lorizio, Ayo P. Doumatey, Alvaro A. Cruz, Harold Watson, Edward T. Naureckas, B. Louise Giles, Ganiyu Arinola, Olumide Sogaolu, Adegoke G. Falade, Nadia N. Hansel, Christopher O. Olopade, Charles N. Rotimi, R. Clive Landis, Camila A. Figueiredo, Eimear E. Kenny, Ingo Ruczinski, Andrew H. Liu, Carole Ober, Margaret A. Taub, Randi K. Johnson, Kathleen C. Barnes, Genevieve L. Wojcik, Rasika A. Mathias
Background Existing asthma polygenic risk scores (PRSs) have minimal validation in African‐ancestry populations, leaving gaps in our understanding of the wide applicability of PRSs. To widen our understanding of the applicability of asthma PRSs, we apply published PRSs in African‐ancestry individuals and quantify the extent to which the PRS‐asthma relationship is mediated by clinical biomarkers and gene‐expression signatures of asthma. Methods We applied 22 PRSs from the PGS Catalog in 673 individuals from the Consortium on Asthma among African‐Ancestry Populations in the Americas (CAAPA) and calculated the percent of the PRS‐asthma relationship that is statistically mediated by clinical and nasal epithelium transcriptomic biomarkers of asthma. Asthma case/control status was defined as ever/never having a doctor's diagnosis of disease. For gene expression mediation analysis, we limited the cases to those with current disease. Results The PRS (PGS001782) created by the Global Biobank Meta‐analysis Initiative ( N = 32,658 individuals of African ancestry) performed the best (ΔAUC = 0.104, AUC = 0.657) adjusted for age, sex, study site, and the first two genetic principal components (PC1‐2). The PRS's effect on asthma was mediated by total IgE (tIgE) (38.8%, p .adj < 0.0002), multi‐allergen ImmunoCAP phadiatop specific IgE (sIgE) (38.7%, p .adj < 0.0002), and eosinophils (7.3%, p .adj = 0.004). Mediation was observed for gene expression modules related to T2 inflammation (21.9%, p .adj < 0.0024), wound healing (11.9%, p .adj = 0.008), and medication response (6.8%, p .adj = 0.049). Conclusion We found the best PRS to be the one derived using the largest sample size and including African‐ancestry individuals. Mediation supports the well‐documented biology of T2 inflammation in asthma as well as pathophysiological components of asthma like wound healing and medication response.
{"title":"Mediation of Polygenic Asthma Risk Through Gene Expression","authors":"Rakesh Natarajan, Brooke Szczesny, Kanika Kanchan, Erika Esquinca, Meher Preethi Boorgula, Sameer Chavan, Monica Campbell, Wendy Lorizio, Ayo P. Doumatey, Alvaro A. Cruz, Harold Watson, Edward T. Naureckas, B. Louise Giles, Ganiyu Arinola, Olumide Sogaolu, Adegoke G. Falade, Nadia N. Hansel, Christopher O. Olopade, Charles N. Rotimi, R. Clive Landis, Camila A. Figueiredo, Eimear E. Kenny, Ingo Ruczinski, Andrew H. Liu, Carole Ober, Margaret A. Taub, Randi K. Johnson, Kathleen C. Barnes, Genevieve L. Wojcik, Rasika A. Mathias","doi":"10.1111/all.70101","DOIUrl":"https://doi.org/10.1111/all.70101","url":null,"abstract":"Background Existing asthma polygenic risk scores (PRSs) have minimal validation in African‐ancestry populations, leaving gaps in our understanding of the wide applicability of PRSs. To widen our understanding of the applicability of asthma PRSs, we apply published PRSs in African‐ancestry individuals and quantify the extent to which the PRS‐asthma relationship is mediated by clinical biomarkers and gene‐expression signatures of asthma. Methods We applied 22 PRSs from the PGS Catalog in 673 individuals from the Consortium on Asthma among African‐Ancestry Populations in the Americas (CAAPA) and calculated the percent of the PRS‐asthma relationship that is statistically mediated by clinical and nasal epithelium transcriptomic biomarkers of asthma. Asthma case/control status was defined as ever/never having a doctor's diagnosis of disease. For gene expression mediation analysis, we limited the cases to those with current disease. Results The PRS (PGS001782) created by the Global Biobank Meta‐analysis Initiative ( <jats:italic>N</jats:italic> = 32,658 individuals of African ancestry) performed the best (ΔAUC = 0.104, AUC = 0.657) adjusted for age, sex, study site, and the first two genetic principal components (PC1‐2). The PRS's effect on asthma was mediated by total IgE (tIgE) (38.8%, <jats:italic>p</jats:italic> .adj < 0.0002), multi‐allergen ImmunoCAP phadiatop specific IgE (sIgE) (38.7%, <jats:italic>p</jats:italic> .adj < 0.0002), and eosinophils (7.3%, <jats:italic>p</jats:italic> .adj = 0.004). Mediation was observed for gene expression modules related to T2 inflammation (21.9%, <jats:italic>p</jats:italic> .adj < 0.0024), wound healing (11.9%, <jats:italic>p</jats:italic> .adj = 0.008), and medication response (6.8%, <jats:italic>p</jats:italic> .adj = 0.049). Conclusion We found the best PRS to be the one derived using the largest sample size and including African‐ancestry individuals. Mediation supports the well‐documented biology of T2 inflammation in asthma as well as pathophysiological components of asthma like wound healing and medication response.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"141 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145680343","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":"Between Healing and Harm: The Two Faces of Acetylcholine in Lung Immunity","authors":"Alessandra Ruiz‐Sánchez, Emilio Nuñez‐Borque, Rodrigo Jiménez‐Saiz","doi":"10.1111/all.70185","DOIUrl":"https://doi.org/10.1111/all.70185","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"56 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145680346","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}
Maria Hartiala,Varpu Elenius,Alicia Aguado Pesquera,Silas Androulakis,Isabella Annesi-Maesano,Artur Badyda,Sicco Brandsma,Ioanna Chatziprodromidou,Goran Gajski,Judith Garcia-Aymerich,Chiara Giorio,Timo Hugg,Jouni J K Jaakkola,Sarah Koch,Pim E G Leonards,Angeliki Matrali,Lisa Melymuk,Natalie Mueller,Adam Muszyński,Jet Opbroek,Inês Paciência,Spyros N Pandis,Sofya Pozdniakova,Aino K Rantala,Sandra Rodríguez Sufuentes,Linda Schenk,Eva Sugeng,Adrià Sunyer-Caldú,Apostolos Vantarakis,Alexander Zherebker,Ernesto Alfaro-Moreno,Pernilla Bohlin Nizzetto,José Fermoso Dominguez,Stylianos Karatzas,Francesco Mureddu,Heidi Salonen,Nikolaos Papadopoulos,Tuomas Jartti,
Indoor air quality (IAQ) is influenced by a wide range of chemical, biological and physical agents that can negatively impact physical, immunological and mental health. Adverse health effects depend on the type and concentration of pollutants, duration of exposure, and individual susceptibility. The availability of data on IAQ is limited, as are standardized approaches for evaluating its health impact. This expert review aims to describe the most important indoor air determinants affecting health, and present the IDEAL cluster, which comprises seven EU-funded scientific projects on the topic of IAQ and human health. Across the IDEAL projects, knowledge is generated on exposure to a wide range of indoor air pollutants, including well-known hazards and more explorative chemical and microbiological determinants. The projects will also contribute to the implementation of low-cost and/or real-time sensors on IAQ, as well as advanced chemical and microbiological analyses, and evaluate various interventions to improve IAQ. Several of them focus on particularly vulnerable groups. Raising public awareness and implementing measures to reduce pollutant levels are essential for safeguarding health, particularly in urban areas with elevated pollution levels.
{"title":"Exposures in Indoor Air Affecting Health.","authors":"Maria Hartiala,Varpu Elenius,Alicia Aguado Pesquera,Silas Androulakis,Isabella Annesi-Maesano,Artur Badyda,Sicco Brandsma,Ioanna Chatziprodromidou,Goran Gajski,Judith Garcia-Aymerich,Chiara Giorio,Timo Hugg,Jouni J K Jaakkola,Sarah Koch,Pim E G Leonards,Angeliki Matrali,Lisa Melymuk,Natalie Mueller,Adam Muszyński,Jet Opbroek,Inês Paciência,Spyros N Pandis,Sofya Pozdniakova,Aino K Rantala,Sandra Rodríguez Sufuentes,Linda Schenk,Eva Sugeng,Adrià Sunyer-Caldú,Apostolos Vantarakis,Alexander Zherebker,Ernesto Alfaro-Moreno,Pernilla Bohlin Nizzetto,José Fermoso Dominguez,Stylianos Karatzas,Francesco Mureddu,Heidi Salonen,Nikolaos Papadopoulos,Tuomas Jartti, ","doi":"10.1111/all.70179","DOIUrl":"https://doi.org/10.1111/all.70179","url":null,"abstract":"Indoor air quality (IAQ) is influenced by a wide range of chemical, biological and physical agents that can negatively impact physical, immunological and mental health. Adverse health effects depend on the type and concentration of pollutants, duration of exposure, and individual susceptibility. The availability of data on IAQ is limited, as are standardized approaches for evaluating its health impact. This expert review aims to describe the most important indoor air determinants affecting health, and present the IDEAL cluster, which comprises seven EU-funded scientific projects on the topic of IAQ and human health. Across the IDEAL projects, knowledge is generated on exposure to a wide range of indoor air pollutants, including well-known hazards and more explorative chemical and microbiological determinants. The projects will also contribute to the implementation of low-cost and/or real-time sensors on IAQ, as well as advanced chemical and microbiological analyses, and evaluate various interventions to improve IAQ. Several of them focus on particularly vulnerable groups. Raising public awareness and implementing measures to reduce pollutant levels are essential for safeguarding health, particularly in urban areas with elevated pollution levels.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"7 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145663943","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":"Development of a Conjugate Vaccine Targeting Human IgE for Long-Term Prevention of Anaphylaxis.","authors":"Vincent Serra,Laurent L Reber","doi":"10.1111/all.70099","DOIUrl":"https://doi.org/10.1111/all.70099","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"157 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664044","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":"Questionnaire Survey on Loquat-Induced Oral Allergy Syndrome in School Children in Yamanashi, Japan.","authors":"Ayumi Shimamura,Reiji Kojima,Hiroki Ishii,Tomokazu Matsuoka,Hisatake Ikeda,Daiju Sakurai","doi":"10.1111/all.70177","DOIUrl":"https://doi.org/10.1111/all.70177","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"57 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664047","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}
Bernardo Sousa-Pinto,Jean Bousquet,Rafael José Vieira,Holger J Schünemann,Torsten Zuberbier,Antonio Bognanni,Alkis Togias,Boleslaw Samolinski,Arunas Valiulis,Sian Williams,Anna Bedbrook,Wienczyslawa Czarlewski,Maria Jose Torres,Mohamed H Shamji,Mário Morais-Almeida,G Walter Canonica,Leticia de Las Vecillas,Mark S Dykewicz,Cristina Jacomelli,Ludger Klimek,Lucas Leemann,Olga Lourenço,Yuliia Palamarchuk,Nikolaos G Papadopoulos,Ana Margarida Pereira,Marine Savouré,Sanna K Toppila-Salmi,Maria Teresa Ventura,Juan José Yepes-Nuñez,Alvaro A Cruz,Giorgio Ciprandi,Bilun Gemicioglu,Mattia Giovannini,Brigita Gradauskiene,Tuomas Jartti,Miloš Jeseňák,Piotr Kuna,Violeta Kvedariene,Désirée E Larenas-Linnemann,Amir Ha Latiff,Yousser Mohammad,Ken Ohta,Padukudru A Mahesh,Isabella Pali-Schöll,Oliver Pfaar,Frederico S Regateiro,Nicolas Roche,Luís Taborda-Barata,Charlotte Suppli Ulrik,Marylin Valentin Rostan,Giovanni Viegi,Luo Zhang,Tari Haahtela,Ivan Cherrez-Ojeda,Juan Carlos Ivancevich,Nikolai Khaltaev,Arzu Yorgancioglu,Baharudin Abdullah,Mona Al-Ahmad,Maryam Ali Al-Nesf,Rita Amaral,Julijana Asllani,Karl-C Bergmann,Jonathan A Bernstein,Michael S Blaiss,Fulvio Braido,Paulo Camargos,Pedro Carreiro-Martins,Thomas Casale,Lorenzo Cecchi,Alessandro Fiocchi,Antonio F M Giuliano,George Christoff,Ieva Cirule,Jaime Correia de Sousa,Elisio M Costa,Stefano Del Giacco,Philippe Devillier,Dejan Dokic,Elham Hossny,Tomohisa Iinuma,Carla Irani,Zhanat Ispayeva,Kaja Julge,Igor Kaidashev,Kazi S Bennoor,Helga Kraxner,Inger Kull,Marek Kulus,Maciej Kupczyk,Andriy Kurchenko,Stefania La Grutta,Neven Miculinic,Lan Le Thi Tuyet,Michael Makris,Branislava Milenkovic,Sang Min Lee,Stephen Montefort,Andre Moreira,Joaquim Mullol,Rachel Nadif,Alla Nakonechna,Hugo E Neffen,Marek Niedoszytko,Dieudonné Nyembue,Robyn E O'Hehir,Ismail Ogulur,Yoshitaka Okamoto,Heidi Olze,Oscar Palomares,Petr Panzner,Vincenzo Patella,Ruby Pawankar,Constantinos Pitsios,Todor A Popov,Francesca Puggioni,Santiago Quirce,Agné Ramonaité,Marysia Recto,Maria Susana Repka-Ramirez,Graham Roberts,Karla Robles-Velasco,Menachem Rottem,Marianella Salapatas,Joaquin Sastre,Nicola Scichilone,Juan-Carlos Sisul,Dirceu Solé,Manuel E Soto-Martinez,Milan Sova,Pongsakorn Tantilipikorn,Ana Todo-Bom,Vladyslav Tsaryk,Ioanna Tsiligianni,Marilyn Urrutia-Pereira,Erkka Valovirta,Tuula Vasankari,Dana Wallace,De Yun Wang,Margitta Worm,Osman M Yusuf,Mihaela Zidarn,Sara Gil-Mata,Manuel Marques-Cruz,Bassam Mahboub,Ignacio J Ansotegui,Antonino Romano,Werner Aberer,Maria Cristina Artesani,Elena Azzolini,Bruno Barreto,Joan Bartra,Sven Becker,Bianca Beghe,Attilio Boner,Ewa Borowiack,Jacques Bouchard,Melisande Bourgoin-Heck,Luisa Brussino,Roland Buhl,José Antonio Castillo-Vizuete,Denis Charpin,Niels H Chavannes,Marta Chełmińska,Lei Cheng,Ekaterine Chkhartishvili,Seong H Cho,Herberto Jose Chong-Neto,Deepa Choudhury,Derek K Chu,Cemal Cingi,Enrico Compalati,Raquel Albuquerque Costa,Olga Mariana Cunha,Biljana Cvetkovski,Victoria Cardona-Dahl,Gennaro D'Amato,Janet Davies,Danilo Di Bona,Sandra N Gonzalez Diaz,Maria V Dimou,Maria Doulaptsi,Renato Ferreira-da-Silva,Radoslaw Gawlik,Mario Calvo-Gil,Ozlem Goksel,Maximiliano R Gómez,Maia Gotua,Christos Grigoreas,Ineta Grisle,Maria Antonieta Guzman,Rachel House Tan,Michael Hyland,Despo Ierodiakonou,Aspasia Karavelia,Paul Keith,Marta Kisiel,Tanja Soklic Kosak,Mitja Kosnik,Ilgim Vardaloglu Koyuncu,Vicky Kritikos,Justyna Litynska,Carlo Lombardi,Gilles Louis,Matteo Martini,Cem Meço,Eris Mesonjesi,Florin Mihaltan,Marcin Moniuszko,Robert N Naclerio,Kari C Nadeau,Sophia Neisinger,Markus Ollert,Michal Ordak,Giovanni Paoletti,Hae-Sim Park,Elena Parmelli,Edgar Arturo Perdomo-Flores,José Miguel Fuentes Pérez,Nhan Pham-Thi,Emmanuel Prokopakis,Inês Ribeiro-Vaz,Giovanni Rolla,Jan Romantowski,Philippe Rombaux,Philip W Rouadi,Maia Rukhadze,Dermot Ryan,Ewelina Sadowska,Daiju Sakurai,Laila Salameh,Faradiba Serpa Sarquis,Elie Serrano,Jane Da Silva,Michael Soyka,Krzysztof Specjalski,Vesna Tomic-Spiric,Katarina Stevanovic,Abirami Subramaniam,Maria Do Ceu Teixeira,Tuuli Thomander,Martina Vachova,Marianne van Hage,Pakit Vichyanond,Martin Wagenmann,Fanny Wai San Ko,Pascal Werminghaus,Paraskevi Vicky Xepapadaki,Yi-Kui Xiang,Qintai Yang,Daniela Rivero Yeverino,Jaron Zuberbier,João A Fonseca
BACKGROUNDAllergic rhinitis (AR) impacts quality of life, work and school productivity. Over the last years, an important body of evidence resulting from mHealth data has led to a better understanding of AR. Such advances have motivated an EAACI-endorsed update of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines (ARIA 2024-2025). This manuscript presents the ARIA 2024-2025 recommendations for intranasal treatments, one of the mainstays for AR management.METHODSThe ARIA 2024-2025 guideline panel issued recommendations following the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) evidence-to-decision framework. Several sources of evidence were used to inform panel judgments and recommendations, including systematic reviews, evaluation of mHealth and pharmacovigilance data, as well as a survey of experts on costs.RESULTSEleven guideline questions concerning intranasal treatments for AR were prioritized, leading to recommendations. Overall, these questions concern the choice between different classes of intranasal medications-most notably, intranasal corticosteroids (INCS), antihistamines (INAH), fixed combinations of INAH+INCS and decongestants-or between different individual medications within each class. Four questions had not been evaluated in previous ARIA guidelines, while for the other three there was a change in the strength or directionality of recommendations. Overall, recommendations point to the suggested use of INAH+INCS over INAH or INCS and INCS over INAH.CONCLUSIONThis ARIA 2024-2025 article supports patients, their caregivers, and healthcare professionals in choosing an intranasal treatment. However, decisions on AR treatment should consider the clinical variability of the disease, patients' values, and the affordability of medications.
{"title":"Allergic Rhinitis and Its Impact on Asthma (ARIA)-EAACI Guidelines-2024-2025 Revision: Part I-Guidelines on Intranasal Treatments.","authors":"Bernardo Sousa-Pinto,Jean Bousquet,Rafael José Vieira,Holger J Schünemann,Torsten Zuberbier,Antonio Bognanni,Alkis Togias,Boleslaw Samolinski,Arunas Valiulis,Sian Williams,Anna Bedbrook,Wienczyslawa Czarlewski,Maria Jose Torres,Mohamed H Shamji,Mário Morais-Almeida,G Walter Canonica,Leticia de Las Vecillas,Mark S Dykewicz,Cristina Jacomelli,Ludger Klimek,Lucas Leemann,Olga Lourenço,Yuliia Palamarchuk,Nikolaos G Papadopoulos,Ana Margarida Pereira,Marine Savouré,Sanna K Toppila-Salmi,Maria Teresa Ventura,Juan José Yepes-Nuñez,Alvaro A Cruz,Giorgio Ciprandi,Bilun Gemicioglu,Mattia Giovannini,Brigita Gradauskiene,Tuomas Jartti,Miloš Jeseňák,Piotr Kuna,Violeta Kvedariene,Désirée E Larenas-Linnemann,Amir Ha Latiff,Yousser Mohammad,Ken Ohta,Padukudru A Mahesh,Isabella Pali-Schöll,Oliver Pfaar,Frederico S Regateiro,Nicolas Roche,Luís Taborda-Barata,Charlotte Suppli Ulrik,Marylin Valentin Rostan,Giovanni Viegi,Luo Zhang,Tari Haahtela,Ivan Cherrez-Ojeda,Juan Carlos Ivancevich,Nikolai Khaltaev,Arzu Yorgancioglu,Baharudin Abdullah,Mona Al-Ahmad,Maryam Ali Al-Nesf,Rita Amaral,Julijana Asllani,Karl-C Bergmann,Jonathan A Bernstein,Michael S Blaiss,Fulvio Braido,Paulo Camargos,Pedro Carreiro-Martins,Thomas Casale,Lorenzo Cecchi,Alessandro Fiocchi,Antonio F M Giuliano,George Christoff,Ieva Cirule,Jaime Correia de Sousa,Elisio M Costa,Stefano Del Giacco,Philippe Devillier,Dejan Dokic,Elham Hossny,Tomohisa Iinuma,Carla Irani,Zhanat Ispayeva,Kaja Julge,Igor Kaidashev,Kazi S Bennoor,Helga Kraxner,Inger Kull,Marek Kulus,Maciej Kupczyk,Andriy Kurchenko,Stefania La Grutta,Neven Miculinic,Lan Le Thi Tuyet,Michael Makris,Branislava Milenkovic,Sang Min Lee,Stephen Montefort,Andre Moreira,Joaquim Mullol,Rachel Nadif,Alla Nakonechna,Hugo E Neffen,Marek Niedoszytko,Dieudonné Nyembue,Robyn E O'Hehir,Ismail Ogulur,Yoshitaka Okamoto,Heidi Olze,Oscar Palomares,Petr Panzner,Vincenzo Patella,Ruby Pawankar,Constantinos Pitsios,Todor A Popov,Francesca Puggioni,Santiago Quirce,Agné Ramonaité,Marysia Recto,Maria Susana Repka-Ramirez,Graham Roberts,Karla Robles-Velasco,Menachem Rottem,Marianella Salapatas,Joaquin Sastre,Nicola Scichilone,Juan-Carlos Sisul,Dirceu Solé,Manuel E Soto-Martinez,Milan Sova,Pongsakorn Tantilipikorn,Ana Todo-Bom,Vladyslav Tsaryk,Ioanna Tsiligianni,Marilyn Urrutia-Pereira,Erkka Valovirta,Tuula Vasankari,Dana Wallace,De Yun Wang,Margitta Worm,Osman M Yusuf,Mihaela Zidarn,Sara Gil-Mata,Manuel Marques-Cruz,Bassam Mahboub,Ignacio J Ansotegui,Antonino Romano,Werner Aberer,Maria Cristina Artesani,Elena Azzolini,Bruno Barreto,Joan Bartra,Sven Becker,Bianca Beghe,Attilio Boner,Ewa Borowiack,Jacques Bouchard,Melisande Bourgoin-Heck,Luisa Brussino,Roland Buhl,José Antonio Castillo-Vizuete,Denis Charpin,Niels H Chavannes,Marta Chełmińska,Lei Cheng,Ekaterine Chkhartishvili,Seong H Cho,Herberto Jose Chong-Neto,Deepa Choudhury,Derek K Chu,Cemal Cingi,Enrico Compalati,Raquel Albuquerque Costa,Olga Mariana Cunha,Biljana Cvetkovski,Victoria Cardona-Dahl,Gennaro D'Amato,Janet Davies,Danilo Di Bona,Sandra N Gonzalez Diaz,Maria V Dimou,Maria Doulaptsi,Renato Ferreira-da-Silva,Radoslaw Gawlik,Mario Calvo-Gil,Ozlem Goksel,Maximiliano R Gómez,Maia Gotua,Christos Grigoreas,Ineta Grisle,Maria Antonieta Guzman,Rachel House Tan,Michael Hyland,Despo Ierodiakonou,Aspasia Karavelia,Paul Keith,Marta Kisiel,Tanja Soklic Kosak,Mitja Kosnik,Ilgim Vardaloglu Koyuncu,Vicky Kritikos,Justyna Litynska,Carlo Lombardi,Gilles Louis,Matteo Martini,Cem Meço,Eris Mesonjesi,Florin Mihaltan,Marcin Moniuszko,Robert N Naclerio,Kari C Nadeau,Sophia Neisinger,Markus Ollert,Michal Ordak,Giovanni Paoletti,Hae-Sim Park,Elena Parmelli,Edgar Arturo Perdomo-Flores,José Miguel Fuentes Pérez,Nhan Pham-Thi,Emmanuel Prokopakis,Inês Ribeiro-Vaz,Giovanni Rolla,Jan Romantowski,Philippe Rombaux,Philip W Rouadi,Maia Rukhadze,Dermot Ryan,Ewelina Sadowska,Daiju Sakurai,Laila Salameh,Faradiba Serpa Sarquis,Elie Serrano,Jane Da Silva,Michael Soyka,Krzysztof Specjalski,Vesna Tomic-Spiric,Katarina Stevanovic,Abirami Subramaniam,Maria Do Ceu Teixeira,Tuuli Thomander,Martina Vachova,Marianne van Hage,Pakit Vichyanond,Martin Wagenmann,Fanny Wai San Ko,Pascal Werminghaus,Paraskevi Vicky Xepapadaki,Yi-Kui Xiang,Qintai Yang,Daniela Rivero Yeverino,Jaron Zuberbier,João A Fonseca","doi":"10.1111/all.70131","DOIUrl":"https://doi.org/10.1111/all.70131","url":null,"abstract":"BACKGROUNDAllergic rhinitis (AR) impacts quality of life, work and school productivity. Over the last years, an important body of evidence resulting from mHealth data has led to a better understanding of AR. Such advances have motivated an EAACI-endorsed update of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines (ARIA 2024-2025). This manuscript presents the ARIA 2024-2025 recommendations for intranasal treatments, one of the mainstays for AR management.METHODSThe ARIA 2024-2025 guideline panel issued recommendations following the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) evidence-to-decision framework. Several sources of evidence were used to inform panel judgments and recommendations, including systematic reviews, evaluation of mHealth and pharmacovigilance data, as well as a survey of experts on costs.RESULTSEleven guideline questions concerning intranasal treatments for AR were prioritized, leading to recommendations. Overall, these questions concern the choice between different classes of intranasal medications-most notably, intranasal corticosteroids (INCS), antihistamines (INAH), fixed combinations of INAH+INCS and decongestants-or between different individual medications within each class. Four questions had not been evaluated in previous ARIA guidelines, while for the other three there was a change in the strength or directionality of recommendations. Overall, recommendations point to the suggested use of INAH+INCS over INAH or INCS and INCS over INAH.CONCLUSIONThis ARIA 2024-2025 article supports patients, their caregivers, and healthcare professionals in choosing an intranasal treatment. However, decisions on AR treatment should consider the clinical variability of the disease, patients' values, and the affordability of medications.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"25 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145644890","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}
BACKGROUNDHeat-not-burn (HnB) tobacco products are marketed as a safer alternative to conventional cigarettes (CC), yet their health effects remain controversial, largely based on industry-funded studies. We aimed to assess lung function in HnB and CC users and examine the mechanistic effects of HnB exposure using animal and in vitro models.METHODSSpirometry data from 650 non-smokers (NS), 293 CC smokers, and 49 HnB users enrolled in the Bialystok-PLUS cohort were analyzed. To investigate underlying mechanisms, a whole-body mouse exposure model was performed with HnB aerosol or 3R4F cigarette smoke, assessing lung transcriptomic profiles (by means of RNA sequencing), lung inflammation (by flow cytometry and histochemical staining), and barrier integrity (by using immunofluorescent staining). Moreover, an in vitro ALI-culture model of human airway epithelial cells was used to validate the mouse experiments. The effect of HnB and CC was assessed through cytotoxic effect (MTT and LDH), inflammatory responses (cytokine release by ELISA), and tight junction proteins (immunofluorescence staining).RESULTSpirometric analysis (FEV1, FVC, VC) revealed no significant overall differences in lung function among HnB users, CC smokers, and non-smokers (NS) in the unadjusted comparison. However, subgroup analyses showed that younger (< 45 years) HnB users and those with shorter smoking histories (< 20 years) already exhibited significantly lower FEV1, FVC, and VC compared to NS and CC smokers. After adjustment for age and smoking-related covariates, HnB users displayed modest but significant reductions in static FEV1 and FVC relative to NS, while no adjusted differences were detected between HnB and CC groups, indicating comparable baseline ventilatory function. Both exposures in mice increased eosinophils and B cell counts by ~2-fold, while decreasing ST2+ CD4+ T cells over 80%, and induced epithelial apoptosis. HnB aerosol selectively reduced basophils by almost 50%. Both HnB and CC exposure in mice caused significant epithelial damage and impaired airway barrier function, evidenced by a ~60% reduction in ZO-1. Transcriptomic analysis revealed that CC smoke triggered a robust inflammatory gene response, whereas HnB aerosol predominantly altered metabolic pathways. In vitro, barrier function was impaired under both conditions, but cytokine secretion increased only after CC smoke exposure.CONCLUSIONDespite different molecular impacts, HnB aerosol exposure induces a level of airway epithelial injury and immune cell infiltration comparable to CC smoke. Our findings challenged the narrative of HnB products being a harmless alternative and highlight their potential to cause significant lung pathology.
{"title":"Heat-Not-Burn Tobacco Aerosols Induce Immune Dysregulation and Barrier Disruption Comparable to Conventional Cigarettes.","authors":"Dilara Karaguzel,Alicja Walewska,Basak Ezgi Sarac,Marlena Tynecka,Kinga Bondarczuk,Agnieszka Tarasik,Dariusz Kisiel,Karolina Partyk,Damian Pogodziński,Bartosz Hanczaruk,Alicja Toczydlowska,Cagla Bicakci,Doga Oztabak,Magdalena Niemira,Adam Kretowski,Marlena Dubatowka,Natalia Ogrodnik,Malgorzata Chlabicz,Pawel Sowa,Karol Kaminski,Marcin Moniuszko,Andrzej Eljaszewicz,Cagatay Karaaslan","doi":"10.1111/all.70174","DOIUrl":"https://doi.org/10.1111/all.70174","url":null,"abstract":"BACKGROUNDHeat-not-burn (HnB) tobacco products are marketed as a safer alternative to conventional cigarettes (CC), yet their health effects remain controversial, largely based on industry-funded studies. We aimed to assess lung function in HnB and CC users and examine the mechanistic effects of HnB exposure using animal and in vitro models.METHODSSpirometry data from 650 non-smokers (NS), 293 CC smokers, and 49 HnB users enrolled in the Bialystok-PLUS cohort were analyzed. To investigate underlying mechanisms, a whole-body mouse exposure model was performed with HnB aerosol or 3R4F cigarette smoke, assessing lung transcriptomic profiles (by means of RNA sequencing), lung inflammation (by flow cytometry and histochemical staining), and barrier integrity (by using immunofluorescent staining). Moreover, an in vitro ALI-culture model of human airway epithelial cells was used to validate the mouse experiments. The effect of HnB and CC was assessed through cytotoxic effect (MTT and LDH), inflammatory responses (cytokine release by ELISA), and tight junction proteins (immunofluorescence staining).RESULTSpirometric analysis (FEV1, FVC, VC) revealed no significant overall differences in lung function among HnB users, CC smokers, and non-smokers (NS) in the unadjusted comparison. However, subgroup analyses showed that younger (< 45 years) HnB users and those with shorter smoking histories (< 20 years) already exhibited significantly lower FEV1, FVC, and VC compared to NS and CC smokers. After adjustment for age and smoking-related covariates, HnB users displayed modest but significant reductions in static FEV1 and FVC relative to NS, while no adjusted differences were detected between HnB and CC groups, indicating comparable baseline ventilatory function. Both exposures in mice increased eosinophils and B cell counts by ~2-fold, while decreasing ST2+ CD4+ T cells over 80%, and induced epithelial apoptosis. HnB aerosol selectively reduced basophils by almost 50%. Both HnB and CC exposure in mice caused significant epithelial damage and impaired airway barrier function, evidenced by a ~60% reduction in ZO-1. Transcriptomic analysis revealed that CC smoke triggered a robust inflammatory gene response, whereas HnB aerosol predominantly altered metabolic pathways. In vitro, barrier function was impaired under both conditions, but cytokine secretion increased only after CC smoke exposure.CONCLUSIONDespite different molecular impacts, HnB aerosol exposure induces a level of airway epithelial injury and immune cell infiltration comparable to CC smoke. Our findings challenged the narrative of HnB products being a harmless alternative and highlight their potential to cause significant lung pathology.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"151 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145644897","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}
Christian Radauer,Gabriele Gadermaier,Richard E Goodman,Alain Jacquet,Uta Jappe,Andreas L Lopata,Anna Pomés,Monika Raulf,Keity S Santos,Josefina Zakzuk,Yuzhu Zhang,Joana Vitte,
The WHO/IUIS Allergen Nomenclature Sub-Committee is an international body of experts that maintains the systematic nomenclature of allergenic proteins by assigning official names to newly identified allergens submitted by researchers. Here, we summarize the data on new allergens approved between 2021 and 2024. The sub-committee assigned names to 112 new allergens with 124 isoallergens/variants as well as 26 new isoallergens/variants of previously named allergens. Most new allergens were respiratory allergens from animals (35 allergens) and plants (25) as well as food allergens from animals (22) and plants (17). Many newly identified allergens reflect globalized allergen exposure and growing research activities outside of Western countries. This is illustrated by allergens from the tropical mite Blomia tropicalis, pollen allergens from tree and weed species native to Asia, and food allergens from regionally important foods such as mango, seafood, silkworm pupae, and natto. The allergen profiles of most relevant sources are well established, but gaps in our knowledge remain, particularly regarding allergens important for populations outside of Europe and North America. The still growing number of known allergens highlights the importance of a consistent, unambiguous allergen nomenclature that evolves with clinical demands and scientific discovery and supports efforts to close existing knowledge gaps.
{"title":"New Allergens Approved by the WHO/IUIS Allergen Nomenclature Sub-Committee in 2021-2024 and Their Significance for Future Diagnostics, Regulation, and Research. An EAACI Task Force Report.","authors":"Christian Radauer,Gabriele Gadermaier,Richard E Goodman,Alain Jacquet,Uta Jappe,Andreas L Lopata,Anna Pomés,Monika Raulf,Keity S Santos,Josefina Zakzuk,Yuzhu Zhang,Joana Vitte, ","doi":"10.1111/all.70166","DOIUrl":"https://doi.org/10.1111/all.70166","url":null,"abstract":"The WHO/IUIS Allergen Nomenclature Sub-Committee is an international body of experts that maintains the systematic nomenclature of allergenic proteins by assigning official names to newly identified allergens submitted by researchers. Here, we summarize the data on new allergens approved between 2021 and 2024. The sub-committee assigned names to 112 new allergens with 124 isoallergens/variants as well as 26 new isoallergens/variants of previously named allergens. Most new allergens were respiratory allergens from animals (35 allergens) and plants (25) as well as food allergens from animals (22) and plants (17). Many newly identified allergens reflect globalized allergen exposure and growing research activities outside of Western countries. This is illustrated by allergens from the tropical mite Blomia tropicalis, pollen allergens from tree and weed species native to Asia, and food allergens from regionally important foods such as mango, seafood, silkworm pupae, and natto. The allergen profiles of most relevant sources are well established, but gaps in our knowledge remain, particularly regarding allergens important for populations outside of Europe and North America. The still growing number of known allergens highlights the importance of a consistent, unambiguous allergen nomenclature that evolves with clinical demands and scientific discovery and supports efforts to close existing knowledge gaps.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"13 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145619808","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}
Type 2 (T2) inflammation is central to allergic disorders. Glycosylation, a post-translational modification, is emerging as a pivotal regulator in T2 inflammation and associated allergic diseases. This review synthesizes current knowledge on glycosylation patterns of key T2 inflammation players, including cytokines, immunoglobulins (e.g., IgE, IgG4) and their receptors, STAT6, mucins, and CTLA-4. We detail how site-specific glycosylation fine-tunes cytokine-receptor interactions, alters signaling pathways, and stabilizes proteins, thereby dictating their bioactivity. Moreover, we examine the enzymatic machinery orchestrating these glycosylation events and the regulatory factors modulating their activity in the context of T2 inflammation. By leveraging these mechanistic insights, we highlight how glycosylation aberrations contribute to food allergy, eosinophilic esophagitis, asthma, allergic rhinitis, and atopic dermatitis, while allergen immunotherapy exploits glycosylation reprogramming (e.g., sialylated IgG4 induction) to restore immune tolerance. Furthermore, we explore the diagnostic and prognostic potential of glycosylation patterns in predicting disease severity and allergen immunotherapy responsiveness, while underscoring the therapeutic promise of targeting glycosylation enzymes or glycan-immune receptor interactions to mitigate T2 inflammation-driven pathologies. A deeper understanding of glycosylation dynamics in T2 inflammation not only enhances our grasp of disease pathogenesis but also opens new avenues for innovative therapeutic interventions.
{"title":"Protein Glycosylation: An Emerging Regulator of Allergic Diseases.","authors":"Pan Li,Xianghong Wang,Ming Zeng,Zheng Liu","doi":"10.1111/all.70171","DOIUrl":"https://doi.org/10.1111/all.70171","url":null,"abstract":"Type 2 (T2) inflammation is central to allergic disorders. Glycosylation, a post-translational modification, is emerging as a pivotal regulator in T2 inflammation and associated allergic diseases. This review synthesizes current knowledge on glycosylation patterns of key T2 inflammation players, including cytokines, immunoglobulins (e.g., IgE, IgG4) and their receptors, STAT6, mucins, and CTLA-4. We detail how site-specific glycosylation fine-tunes cytokine-receptor interactions, alters signaling pathways, and stabilizes proteins, thereby dictating their bioactivity. Moreover, we examine the enzymatic machinery orchestrating these glycosylation events and the regulatory factors modulating their activity in the context of T2 inflammation. By leveraging these mechanistic insights, we highlight how glycosylation aberrations contribute to food allergy, eosinophilic esophagitis, asthma, allergic rhinitis, and atopic dermatitis, while allergen immunotherapy exploits glycosylation reprogramming (e.g., sialylated IgG4 induction) to restore immune tolerance. Furthermore, we explore the diagnostic and prognostic potential of glycosylation patterns in predicting disease severity and allergen immunotherapy responsiveness, while underscoring the therapeutic promise of targeting glycosylation enzymes or glycan-immune receptor interactions to mitigate T2 inflammation-driven pathologies. A deeper understanding of glycosylation dynamics in T2 inflammation not only enhances our grasp of disease pathogenesis but also opens new avenues for innovative therapeutic interventions.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"4 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145613350","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：