Pub Date : 2025-02-03eCollection Date: 2024-01-01DOI: 10.3389/falgy.2024.1531788
G K Scadding, D M Conti, S Scheire, V Backer, M Blaiss, L O Cardell, W De Yun, A K Ellis, W Fokkens, A T Fox, T Gilbert Kruz, S Halken, P W Hellings, V Hox, L Kalogjera, S Lau, S Marinho, M McDonald, R Mösges, J Mullol, S Nasser, R Pawankar, D Price, D Ryan, G Scadding, P Smith, M Sosa Kostrábová, M Vazquez-Ortiz, U Wahn, L Zhang, P Gevaert
Allergic rhinitis (AR), the most prevalent immunological disease, affects approximately 400 million individuals globally and can significantly impact quality of life (QoL). Despite nearly 25 years of guidelines, AR remains largely under- diagnosed, suboptimally treated and poorly controlled. In the light of new knowledge and treatment options, there is a necessity to update or revise fundamental AR definitions to facilitate communication across diverse specialties engaged in its treatment and to improve patient care. The European Forum for Research and Education in Allergy and Airway Diseases (EUFOREA) convened a meeting of experts and patient representatives to deliberate the optimal methodology for measuring AR treatment responses and establishing novel treatment goals. This paper presents a consensus on revised AR definitions, including control, severe allergic rhinoconjunctivitis (SARC), refractory severe allergic rhinoconjunctivitis (R-SARC), remission, resolution, improvement, exacerbation, treatable traits (TTs), treat to target, relapse, progression, disease modification, and prevention.
{"title":"EUFOREA meeting on defining disease states in allergic rhinitis: towards a unified language in AR.","authors":"G K Scadding, D M Conti, S Scheire, V Backer, M Blaiss, L O Cardell, W De Yun, A K Ellis, W Fokkens, A T Fox, T Gilbert Kruz, S Halken, P W Hellings, V Hox, L Kalogjera, S Lau, S Marinho, M McDonald, R Mösges, J Mullol, S Nasser, R Pawankar, D Price, D Ryan, G Scadding, P Smith, M Sosa Kostrábová, M Vazquez-Ortiz, U Wahn, L Zhang, P Gevaert","doi":"10.3389/falgy.2024.1531788","DOIUrl":"https://doi.org/10.3389/falgy.2024.1531788","url":null,"abstract":"<p><p>Allergic rhinitis (AR), the most prevalent immunological disease, affects approximately 400 million individuals globally and can significantly impact quality of life (QoL). Despite nearly 25 years of guidelines, AR remains largely under- diagnosed, suboptimally treated and poorly controlled. In the light of new knowledge and treatment options, there is a necessity to update or revise fundamental AR definitions to facilitate communication across diverse specialties engaged in its treatment and to improve patient care. The European Forum for Research and Education in Allergy and Airway Diseases (EUFOREA) convened a meeting of experts and patient representatives to deliberate the optimal methodology for measuring AR treatment responses and establishing novel treatment goals. This paper presents a consensus on revised AR definitions, including control, severe allergic rhinoconjunctivitis (SARC), refractory severe allergic rhinoconjunctivitis (R-SARC), remission, resolution, improvement, exacerbation, treatable traits (TTs), treat to target, relapse, progression, disease modification, and prevention.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"5 ","pages":"1531788"},"PeriodicalIF":3.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11830706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-30eCollection Date: 2025-01-01DOI: 10.3389/falgy.2025.1529071
Jacek Plichta, Michał Panek
Transforming growth factor beta (TGF-β) is a pluripotent cytokine expressed by all cells of the human body which plays important roles in maintaining homeostasis and allowing for proper individual development. Disturbances in TGF-β signaling contribute to the development of many diseases and disorders, including cancer and organ fibrosis. One of the diseases with the best-characterized correlation between TGF-β action and etiopathogenesis is asthma. Asthma is the most common chronic inflammatory disease of the lower and upper respiratory tract, characterized by bronchial hyperresponsiveness to a number of environmental factors, leading to bronchospasm and reversible limitation of expiratory flow. TGF-β, in particular TGF-β1, is a key factor in the etiopathogenesis of asthma. TGF-β1 concentration in bronchoalveolar lavage fluid samples is elevated in atopic asthma, and TGF-β expression is increased in asthmatic bronchial samples. The expression of all TGF-β isoforms is affected by a number of single nucleotide polymorphisms found in the genes encoding these cytokines. Some of the SNPs that alter the level of TGF-β expression may be associated with the occurrence and severity of symptoms of asthma and other diseases. The TGF-β gene polymorphisms, which are the subject of this paper, are potential diagnostic factors. If properly used, these polymorphisms can facilitate the early and precise diagnosis of asthma, allowing for the introduction of appropriate therapy and reduction of asthma exacerbation frequency.
{"title":"Role of the TGF-β cytokine and its gene polymorphisms in asthma etiopathogenesis.","authors":"Jacek Plichta, Michał Panek","doi":"10.3389/falgy.2025.1529071","DOIUrl":"10.3389/falgy.2025.1529071","url":null,"abstract":"<p><p>Transforming growth factor beta (TGF-β) is a pluripotent cytokine expressed by all cells of the human body which plays important roles in maintaining homeostasis and allowing for proper individual development. Disturbances in TGF-β signaling contribute to the development of many diseases and disorders, including cancer and organ fibrosis. One of the diseases with the best-characterized correlation between TGF-β action and etiopathogenesis is asthma. Asthma is the most common chronic inflammatory disease of the lower and upper respiratory tract, characterized by bronchial hyperresponsiveness to a number of environmental factors, leading to bronchospasm and reversible limitation of expiratory flow. TGF-β, in particular TGF-β1, is a key factor in the etiopathogenesis of asthma. TGF-β1 concentration in bronchoalveolar lavage fluid samples is elevated in atopic asthma, and TGF-β expression is increased in asthmatic bronchial samples. The expression of all TGF-β isoforms is affected by a number of single nucleotide polymorphisms found in the genes encoding these cytokines. Some of the SNPs that alter the level of TGF-β expression may be associated with the occurrence and severity of symptoms of asthma and other diseases. The TGF-β gene polymorphisms, which are the subject of this paper, are potential diagnostic factors. If properly used, these polymorphisms can facilitate the early and precise diagnosis of asthma, allowing for the introduction of appropriate therapy and reduction of asthma exacerbation frequency.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"6 ","pages":"1529071"},"PeriodicalIF":3.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11821632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-29eCollection Date: 2025-01-01DOI: 10.3389/falgy.2025.1544496
Heinrich C Weber, Gaylene L Bassett, Sukhwinder S Sohal, Sarah J Prior
Introduction: The prevalence of childhood food allergies is escalating, with Australia notably affected. Research primarily originates from urban centres, leaving rural areas underrepresented. This study examines food allergy prevalence among 1,052 grade 1 and 2 children in regional and rural Tasmania.
Method: Diagnosis relied on validated parental self-reports and identified anaphylaxis by symptoms coupled with breathing difficulties.
Results: The median participant age was 8.1 years. Food allergy prevalence stood at 8.5% (n = 89), with cow's milk, peanuts/nuts, and eggs as primary allergens. Anaphylaxis prevalence was 18.0% (n = 16) of participants with food allergies, predominantly triggered by peanuts/nuts, eggs, and shellfish.
Conclusion: The study delves into reactions to non-allergenic foods and associated avoidance leading to increased morbidity. This report contributes valuable insights to the insufficiently documented landscape of food allergy prevalence, shedding light on a poorly described aspect.
{"title":"Self-reported food allergies in early childhood in rural Australia.","authors":"Heinrich C Weber, Gaylene L Bassett, Sukhwinder S Sohal, Sarah J Prior","doi":"10.3389/falgy.2025.1544496","DOIUrl":"10.3389/falgy.2025.1544496","url":null,"abstract":"<p><strong>Introduction: </strong>The prevalence of childhood food allergies is escalating, with Australia notably affected. Research primarily originates from urban centres, leaving rural areas underrepresented. This study examines food allergy prevalence among 1,052 grade 1 and 2 children in regional and rural Tasmania.</p><p><strong>Method: </strong>Diagnosis relied on validated parental self-reports and identified anaphylaxis by symptoms coupled with breathing difficulties.</p><p><strong>Results: </strong>The median participant age was 8.1 years. Food allergy prevalence stood at 8.5% (<i>n</i> = 89), with cow's milk, peanuts/nuts, and eggs as primary allergens. Anaphylaxis prevalence was 18.0% (<i>n</i> = 16) of participants with food allergies, predominantly triggered by peanuts/nuts, eggs, and shellfish.</p><p><strong>Conclusion: </strong>The study delves into reactions to non-allergenic foods and associated avoidance leading to increased morbidity. This report contributes valuable insights to the insufficiently documented landscape of food allergy prevalence, shedding light on a poorly described aspect.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"6 ","pages":"1544496"},"PeriodicalIF":3.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11813859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Asthma has an annual increasing morbidity rate and imposes a heavy social burden on public healthcare systems. The aim of this study was to use machine learning to identify asthma-specific genes for the prediction and diagnosis of asthma.
Methods: Differentially expressed genes (DEGs) related to asthma were identified by examining public sequencing data from the Gene Expression Omnibus, coupled with the support vector machine recursive feature elimination and least absolute shrinkage and selection operator regression model. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene set enrichment analysis and correlation analyses between gene and immune cell levels were performed. An ovalbumin-induced asthma mouse model was established, and eukaryotic reference transcriptome high-throughput sequencing was performed to identify genes expressed in mouse lung tissues.
Results: Thirteen specific asthma genes were obtained from our dataset analysis (LOC100132287, CEACAM5, PRR4, CPA3, POSTN, LYPD2, TCN1, SCGB3A1, NOS2, CLCA1, TPSAB1, CST1, and C7orf26). The GO analysis demonstrated that DEGs linked to asthma were primarily related to positive regulation of guanylate cyclase activity, gpi anchor binding, peptidase activity and arginine binding. The renin-angiotensin system, arginine biosynthesis and arginine and proline metabolism were the key KEGG pathways of DEGs. Additionally, the genes CEACAM5, PRR4, CPA3, POSTN, CLCA1, and CST1 expression levels were positively associated with plasma cells and resting mast cells. The mouse model revealed elevated nos2 and clca1 expression in the asthmatic mouse group compared with that in normal mice, which was consistent with the findings in asthmatic patients.
Discussion: This study identified new marker genes for the prediction and diagnosis of asthma, which can be further validated and applied clinically.
{"title":"Machine learning-based screening of asthma biomarkers and related immune infiltration.","authors":"Xiaoying Zhong, Jingjing Song, Changyu Lei, Xiaoming Wang, Yufei Wang, Jiahui Yu, Wei Dai, Xinyi Xu, Junwen Fan, Xiaodong Xia, Weixi Zhang","doi":"10.3389/falgy.2025.1506608","DOIUrl":"https://doi.org/10.3389/falgy.2025.1506608","url":null,"abstract":"<p><strong>Introduction: </strong>Asthma has an annual increasing morbidity rate and imposes a heavy social burden on public healthcare systems. The aim of this study was to use machine learning to identify asthma-specific genes for the prediction and diagnosis of asthma.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) related to asthma were identified by examining public sequencing data from the Gene Expression Omnibus, coupled with the support vector machine recursive feature elimination and least absolute shrinkage and selection operator regression model. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene set enrichment analysis and correlation analyses between gene and immune cell levels were performed. An ovalbumin-induced asthma mouse model was established, and eukaryotic reference transcriptome high-throughput sequencing was performed to identify genes expressed in mouse lung tissues.</p><p><strong>Results: </strong>Thirteen specific asthma genes were obtained from our dataset analysis (<i>LOC100132287</i>, <i>CEACAM5</i>, <i>PRR4</i>, <i>CPA3</i>, <i>POSTN</i>, <i>LYPD2</i>, <i>TCN1</i>, <i>SCGB3A1</i>, <i>NOS2</i>, <i>CLCA1</i>, <i>TPSAB1</i>, <i>CST1</i>, and <i>C7orf26</i>). The GO analysis demonstrated that DEGs linked to asthma were primarily related to positive regulation of guanylate cyclase activity, gpi anchor binding, peptidase activity and arginine binding. The renin-angiotensin system, arginine biosynthesis and arginine and proline metabolism were the key KEGG pathways of DEGs. Additionally, the genes <i>CEACAM5</i>, <i>PRR4</i>, <i>CPA3</i>, <i>POSTN</i>, <i>CLCA1</i>, and <i>CST1</i> expression levels were positively associated with plasma cells and resting mast cells. The mouse model revealed elevated <i>nos2</i> and <i>clca1</i> expression in the asthmatic mouse group compared with that in normal mice, which was consistent with the findings in asthmatic patients.</p><p><strong>Discussion: </strong>This study identified new marker genes for the prediction and diagnosis of asthma, which can be further validated and applied clinically.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"6 ","pages":"1506608"},"PeriodicalIF":3.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11831286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-24eCollection Date: 2025-01-01DOI: 10.3389/falgy.2025.1535103
Susan B H Propst, Dorothea K Thompson
Gastrointestinal (GI) disturbances such as abdominal pain, nausea, and diarrhea are infrequently attributed to food allergies as an initial diagnosis in the absence of more traditional allergic reactions like hives, angioedema, or anaphylaxis. Alpha-gal syndrome (AGS) is an atypical and under-recognized allergy characterized by a delayed hypersensitivity reaction to the oligosaccharide galactose-α-1,3-galactose, a carbohydrate found in non-primate mammalian meat and derived products. This review of the current literature on AGS focuses on GI manifestations and diagnostic challenges. While clinical presentations of AGS vary widely, predominant or isolated GI symptoms, when manifested, can overlap with other disorders, thus making a timely and accurate diagnosis challenging. Here we provide an updated review of the epidemiology, pathophysiology, clinical presentation, and management of AGS. Current diagnostic approaches, treatment strategies, and areas requiring further research are also discussed.
{"title":"Alpha-gal syndrome and the gastrointestinal reaction: a narrative review.","authors":"Susan B H Propst, Dorothea K Thompson","doi":"10.3389/falgy.2025.1535103","DOIUrl":"10.3389/falgy.2025.1535103","url":null,"abstract":"<p><p>Gastrointestinal (GI) disturbances such as abdominal pain, nausea, and diarrhea are infrequently attributed to food allergies as an initial diagnosis in the absence of more traditional allergic reactions like hives, angioedema, or anaphylaxis. Alpha-gal syndrome (AGS) is an atypical and under-recognized allergy characterized by a delayed hypersensitivity reaction to the oligosaccharide galactose-α-1,3-galactose, a carbohydrate found in non-primate mammalian meat and derived products. This review of the current literature on AGS focuses on GI manifestations and diagnostic challenges. While clinical presentations of AGS vary widely, predominant or isolated GI symptoms, when manifested, can overlap with other disorders, thus making a timely and accurate diagnosis challenging. Here we provide an updated review of the epidemiology, pathophysiology, clinical presentation, and management of AGS. Current diagnostic approaches, treatment strategies, and areas requiring further research are also discussed.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"6 ","pages":"1535103"},"PeriodicalIF":3.3,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11802538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143384326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-23eCollection Date: 2024-01-01DOI: 10.3389/falgy.2024.1451296
Luis Felipe Ensina, Larissa Brandão, Luisa Karla Arruda, Faradiba Sarquis Serpa, Régis Albuquerque Campos, Solange Rodrigues Oliveira Valle, Paulo Ricardo Criado, Sarbjit Singh Saini, Roberta Fachini Jardim Criado
This multicenter study aimed to explore whether baseline total immunoglobulin E (IgE) levels could predict omalizumab response in chronic spontaneous urticaria (CSU) patients. Refractory CSU patients, treated with omalizumab after failing second-generation H1-antihistamines, were analyzed retrospectively across seven centers in Brazil. The study assessed total IgE levels at baseline, comparing responders to non-responders and considering complete and partial responses. The results showed a significant reduction in CSU symptoms post-treatment. Non-responders had lower baseline IgE levels. A sensitivity of 67.8% and specificity of 93.3% for predicting a response were found at an IgE level of 59.5 IU/ml. Similar values were observed for complete responders. Notably, a baseline IgE level lower than 59.5 IU/ml may indicate late responders. The study underscores the potential of baseline IgE levels as a predictive biomarker for omalizumab response in CSU patients. Further research, incorporating diverse populations and analyzing response variables, is warranted to validate these findings.
{"title":"IgE as a predictor to omalizumab response in patients with chronic spontaneous urticaria.","authors":"Luis Felipe Ensina, Larissa Brandão, Luisa Karla Arruda, Faradiba Sarquis Serpa, Régis Albuquerque Campos, Solange Rodrigues Oliveira Valle, Paulo Ricardo Criado, Sarbjit Singh Saini, Roberta Fachini Jardim Criado","doi":"10.3389/falgy.2024.1451296","DOIUrl":"10.3389/falgy.2024.1451296","url":null,"abstract":"<p><p>This multicenter study aimed to explore whether baseline total immunoglobulin E (IgE) levels could predict omalizumab response in chronic spontaneous urticaria (CSU) patients. Refractory CSU patients, treated with omalizumab after failing second-generation H1-antihistamines, were analyzed retrospectively across seven centers in Brazil. The study assessed total IgE levels at baseline, comparing responders to non-responders and considering complete and partial responses. The results showed a significant reduction in CSU symptoms post-treatment. Non-responders had lower baseline IgE levels. A sensitivity of 67.8% and specificity of 93.3% for predicting a response were found at an IgE level of 59.5 IU/ml. Similar values were observed for complete responders. Notably, a baseline IgE level lower than 59.5 IU/ml may indicate late responders. The study underscores the potential of baseline IgE levels as a predictive biomarker for omalizumab response in CSU patients. Further research, incorporating diverse populations and analyzing response variables, is warranted to validate these findings.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"5 ","pages":"1451296"},"PeriodicalIF":3.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11798913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-23eCollection Date: 2024-01-01DOI: 10.3389/falgy.2024.1473902
Yoko Kataoka
Thymus and activation-regulated chemokine (TARC; CCL17) is a T-helper-2 chemokine that reflects atopic dermatitis (AD) disease activity. Since 2008, serum TARC levels have been commercially measured in Japan, and clinical experience has shown the usefulness of TARC. The fallacy that eczema is always visible often hinders successful treatment, when there is subclinical inflammation which is inferable from the TARC level. AD treatment has entered a new era with higher therapeutic efficacy. TARC has a different meaning than it did previously, and its significance and limitations are discussed. First, a more appropriate topical therapy monitoring TARC would be useful in selecting truly necessitated patients for expensive new therapies. Dupilumab quickly lowers serum TARC before clinical improvement, and its normalization is not a criterion for dose reduction. However, in some severe cases, TARC may help determine whether to continue treatment. During treatment with JAK inhibitors, serum TARC levels are often elevated and may be abnormally high, leading to the exacerbation of dermatitis. Prurigo nodularis is divided into two types associated with elevated and normal TARC levels, which may aid in the selection of therapeutic agents. In this new era, TARC remains a useful biomarker for more accurate drug selection and the determination of therapeutic efficacy; Currently, in clinical trials of AD, all outcome measurements depend on the clinical score; however the use of a biomarker, such as TARC, as a secondary outcome measure will clarify the characteristics of each drug and the pathophysiological conditions for which it is expected to be effective.
{"title":"Thymus and activation-regulated chemokine (CCL17) as a clinical biomarker in atopic dermatitis: significance and limitations in the new treatment era.","authors":"Yoko Kataoka","doi":"10.3389/falgy.2024.1473902","DOIUrl":"10.3389/falgy.2024.1473902","url":null,"abstract":"<p><p>Thymus and activation-regulated chemokine (TARC; CCL17) is a T-helper-2 chemokine that reflects atopic dermatitis (AD) disease activity. Since 2008, serum TARC levels have been commercially measured in Japan, and clinical experience has shown the usefulness of TARC. The fallacy that eczema is always visible often hinders successful treatment, when there is subclinical inflammation which is inferable from the TARC level. AD treatment has entered a new era with higher therapeutic efficacy. TARC has a different meaning than it did previously, and its significance and limitations are discussed. First, a more appropriate topical therapy monitoring TARC would be useful in selecting truly necessitated patients for expensive new therapies. Dupilumab quickly lowers serum TARC before clinical improvement, and its normalization is not a criterion for dose reduction. However, in some severe cases, TARC may help determine whether to continue treatment. During treatment with JAK inhibitors, serum TARC levels are often elevated and may be abnormally high, leading to the exacerbation of dermatitis. Prurigo nodularis is divided into two types associated with elevated and normal TARC levels, which may aid in the selection of therapeutic agents. In this new era, TARC remains a useful biomarker for more accurate drug selection and the determination of therapeutic efficacy; Currently, in clinical trials of AD, all outcome measurements depend on the clinical score; however the use of a biomarker, such as TARC, as a secondary outcome measure will clarify the characteristics of each drug and the pathophysiological conditions for which it is expected to be effective.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"5 ","pages":"1473902"},"PeriodicalIF":3.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11799291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-23eCollection Date: 2025-01-01DOI: 10.3389/falgy.2025.1533928
Yun-Ho Kim, Chan-Ho Park, Ju Myung Kim, Yeo Cho Yoon
Background: Respiratory allergy is a serious respiratory disorder characterized by inflammation, mucus hypersecretion, and airway tissue sclerosis. Disruption of the T helper 1 (Th1) and T helper 2 (Th2) immune systems by stimuli induced by house dust mites (HDM) and fine particulate matter leads to the secretion of various inflammatory cytokines, resulting in immune respiratory diseases characterized by airway inflammation. Chitooligosaccharides (COS) are known for their antioxidant and anti-inflammatory properties.
Methods: Human airway epithelial cells (BEAS-2B) were cultured in DMEM/F12 medium containing COS at concentrations of 25-100 µg/ml for 24 h. No intracellular toxicity was observed up to 1,000 µg/ml. Cell experiments were conducted at COS concentrations below 100 µg/ml, while animal experiments were performed at concentrations below 100 mg/kg body weight for 4 weeks. Samples of right lung tissue obtained from the experimental animals were used for gene and protein expression analysis, whereas samples of contralateral lung tissue were used for immunohistochemical analysis.
Results: COS regulated Th1 immunity by inhibiting major cytokines, including inflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), in BEAS-2B cells. In the HDM-induced allergic respiratory model, COS suppressed the infiltration of inflammatory cells around the airways and inhibited the mRNA expression of Th1 immune cytokines in lung tissues, while also reducing the expression of nuclear factor kappa B (NF-κB)-related proteins. Furthermore, the results confirmed the suppression of the levels of immunoglobulin E (IgE) in the blood secreted by mast cells activated by HDM, which led to a reduction in allergic mucus hypersecretion and airway sclerosis.
Conclusion: In summary, COS are thought to improve airway resistance by alleviating inflammatory allergic respiratory diseases caused by HDM and are regarded as substances that regulate the balance of the Th1 and Th2 immune systems in epithelial cells affected by mucus hypersecretion.
{"title":"Chitooligosaccharides suppress airway inflammation, fibrosis, and mucus hypersecretion in a house dust mite-induced allergy model.","authors":"Yun-Ho Kim, Chan-Ho Park, Ju Myung Kim, Yeo Cho Yoon","doi":"10.3389/falgy.2025.1533928","DOIUrl":"10.3389/falgy.2025.1533928","url":null,"abstract":"<p><strong>Background: </strong>Respiratory allergy is a serious respiratory disorder characterized by inflammation, mucus hypersecretion, and airway tissue sclerosis. Disruption of the T helper 1 (Th1) and T helper 2 (Th2) immune systems by stimuli induced by house dust mites (HDM) and fine particulate matter leads to the secretion of various inflammatory cytokines, resulting in immune respiratory diseases characterized by airway inflammation. Chitooligosaccharides (COS) are known for their antioxidant and anti-inflammatory properties.</p><p><strong>Methods: </strong>Human airway epithelial cells (BEAS-2B) were cultured in DMEM/F12 medium containing COS at concentrations of 25-100 µg/ml for 24 h. No intracellular toxicity was observed up to 1,000 µg/ml. Cell experiments were conducted at COS concentrations below 100 µg/ml, while animal experiments were performed at concentrations below 100 mg/kg body weight for 4 weeks. Samples of right lung tissue obtained from the experimental animals were used for gene and protein expression analysis, whereas samples of contralateral lung tissue were used for immunohistochemical analysis.</p><p><strong>Results: </strong>COS regulated Th1 immunity by inhibiting major cytokines, including inflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), in BEAS-2B cells. In the HDM-induced allergic respiratory model, COS suppressed the infiltration of inflammatory cells around the airways and inhibited the mRNA expression of Th1 immune cytokines in lung tissues, while also reducing the expression of nuclear factor kappa B (NF-κB)-related proteins. Furthermore, the results confirmed the suppression of the levels of immunoglobulin E (IgE) in the blood secreted by mast cells activated by HDM, which led to a reduction in allergic mucus hypersecretion and airway sclerosis.</p><p><strong>Conclusion: </strong>In summary, COS are thought to improve airway resistance by alleviating inflammatory allergic respiratory diseases caused by HDM and are regarded as substances that regulate the balance of the Th1 and Th2 immune systems in epithelial cells affected by mucus hypersecretion.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"6 ","pages":"1533928"},"PeriodicalIF":3.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11799285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143384327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-21eCollection Date: 2024-01-01DOI: 10.3389/falgy.2024.1463867
Maria V Medeleanu, Myrtha E Reyna, Darlene L Y Dai, Geoffrey L Winsor, Fiona S L Brinkman, Rahul Verma, Ella Nugent, Nashita Riaz, Elinor Simons, Piushkumar J Mandhane, Meghan B Azad, Stuart E Turvey, Theo J Moraes, Padmaja Subbarao
Objective: Lower respiratory tract infections (LRTIs) in early life are one of the strongest risk factors for childhood asthma and are often treated with systemic antibiotics (IV or oral). We aimed to explore the association between early-life LRTIs and systemic antibiotics on asthma development and the potential mediating role of antibiotics in this relationship.
Methods: Data were collected as part of the longitudinal, general Canadian population CHILD Study. LRTIs during the first 18 months of life were identified through parental symptom report at regular study visits. Systemic antibiotic use was defined as at least one dose of oral/intravenous antibiotics between birth and the 18-month visit and were further categorized by indication as either given for a respiratory indication (upper or lower respiratory symptoms) or non-respiratory indication. Asthma was diagnosed by in-study pediatricians at the 5-year study visit. Adjusted logistic regression models and mediation analyses via systemic antibiotics use were performed.
Results: Among 2,073 participants included in our analysis, 72 (4.9%) had asthma age 5, and 609 (29.3%) used systemic antibiotics before the 18-month visit. Among children who had taken antibiotics, 61.6% also had an LRTI in that period compared to 49.7% among children without exposure to systemic antibiotics (p < .001). Moderate-severe LRTIs before age 18 months were associated with higher odds of 5-year asthma [aOR 4.12 (95%CI 2.04-7.95) p < .001]. Antibiotics taken for respiratory indications were associated with higher odds of asthma at age 5 [aOR 2.36 (95%CI 1.59-3.48) p < .001]. Children who received systemic antibiotics for only non-respiratory indications during the first 18 months of life were not associated with increased odds of asthma [aOR 1.08 (95%CI 0.44-2.30) p = .851]. Using mediation analysis, 21.7% of the association between LRTI and asthma is estimated to be mediated through use of early-life systemic antibiotics. However, a significant direct effect of moderate-to-severe LRTIs on asthma risk remained in adjusted mediation models (p = .014).
Conclusion: Through mediation modeling we estimate that the increased risk of asthma at age 5 that is associated with moderate-severe LRTIs in infancy may be partially mediated by systemic antibiotics taken during the first 18 months of life. This underscores the importance of public health strategies focused on antibiotic stewardship and reducing early life LRTIs to mitigate asthma risk.
{"title":"Exploring the potential mediating role of systemic antibiotics in the association between early-life lower respiratory tract infections and asthma at age 5 in the CHILD study.","authors":"Maria V Medeleanu, Myrtha E Reyna, Darlene L Y Dai, Geoffrey L Winsor, Fiona S L Brinkman, Rahul Verma, Ella Nugent, Nashita Riaz, Elinor Simons, Piushkumar J Mandhane, Meghan B Azad, Stuart E Turvey, Theo J Moraes, Padmaja Subbarao","doi":"10.3389/falgy.2024.1463867","DOIUrl":"10.3389/falgy.2024.1463867","url":null,"abstract":"<p><strong>Objective: </strong>Lower respiratory tract infections (LRTIs) in early life are one of the strongest risk factors for childhood asthma and are often treated with systemic antibiotics (IV or oral). We aimed to explore the association between early-life LRTIs and systemic antibiotics on asthma development and the potential mediating role of antibiotics in this relationship.</p><p><strong>Methods: </strong>Data were collected as part of the longitudinal, general Canadian population CHILD Study. LRTIs during the first 18 months of life were identified through parental symptom report at regular study visits. Systemic antibiotic use was defined as at least one dose of oral/intravenous antibiotics between birth and the 18-month visit and were further categorized by indication as either given for a respiratory indication (upper or lower respiratory symptoms) or non-respiratory indication. Asthma was diagnosed by in-study pediatricians at the 5-year study visit. Adjusted logistic regression models and mediation analyses via systemic antibiotics use were performed.</p><p><strong>Results: </strong>Among 2,073 participants included in our analysis, 72 (4.9%) had asthma age 5, and 609 (29.3%) used systemic antibiotics before the 18-month visit. Among children who had taken antibiotics, 61.6% also had an LRTI in that period compared to 49.7% among children without exposure to systemic antibiotics (<i>p</i> < .001). Moderate-severe LRTIs before age 18 months were associated with higher odds of 5-year asthma [aOR 4.12 (95%CI 2.04-7.95) <i>p</i> < .001]. Antibiotics taken for respiratory indications were associated with higher odds of asthma at age 5 [aOR 2.36 (95%CI 1.59-3.48) <i>p</i> < .001]. Children who received systemic antibiotics for only non-respiratory indications during the first 18 months of life were not associated with increased odds of asthma [aOR 1.08 (95%CI 0.44-2.30) <i>p</i> = .851]. Using mediation analysis, 21.7% of the association between LRTI and asthma is estimated to be mediated through use of early-life systemic antibiotics. However, a significant direct effect of moderate-to-severe LRTIs on asthma risk remained in adjusted mediation models (<i>p</i> = .014).</p><p><strong>Conclusion: </strong>Through mediation modeling we estimate that the increased risk of asthma at age 5 that is associated with moderate-severe LRTIs in infancy may be partially mediated by systemic antibiotics taken during the first 18 months of life. This underscores the importance of public health strategies focused on antibiotic stewardship and reducing early life LRTIs to mitigate asthma risk.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"5 ","pages":"1463867"},"PeriodicalIF":3.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-21eCollection Date: 2024-01-01DOI: 10.3389/falgy.2024.1472673
Claudia Felicia Pop, Daniela Rajka, Ioana Corina Bocsan, Petronela Alina Coblisan, Gabriela Edita Ichim, Anna Lazar, Paraschiva Chereches-Panta
The prevalence of food allergy (FA) varies worldwide with an increasing rate in the last decades. Data of self-reported FA have been recorded by most European countries, the US, Canada and Australia, but not Romania. The aim of this study is to analyze the prevalence and severity of FA and to assess the extent of information the medical and teaching staff in schools have on students' medical history.
Methods: A cross-sectional survey was performed in schoolchildren from Cluj-Napoca, Romania, using an online questionnaire delivered to their parents.
Results and conclusions: Seven hundred and eight individuals completed the entire questionnaire. The prevalence of self-reported FA was 8.9%, 28.6% presented food-induced angioedema and 38.1% required ER presentation. Cow milk (36.5%), egg (9.5%), strawberry (20.6%) and nuts (2.7%)were the most frequent culprit foods. The lack of an appropriate and accurate communication with the medical and teaching staff in the school suggest the requirement for further measures for parents and children educations regarding food allergy detection and management.
{"title":"Insights into self-reported food allergies in Romanian schoolchildren.","authors":"Claudia Felicia Pop, Daniela Rajka, Ioana Corina Bocsan, Petronela Alina Coblisan, Gabriela Edita Ichim, Anna Lazar, Paraschiva Chereches-Panta","doi":"10.3389/falgy.2024.1472673","DOIUrl":"10.3389/falgy.2024.1472673","url":null,"abstract":"<p><p>The prevalence of food allergy (FA) varies worldwide with an increasing rate in the last decades. Data of self-reported FA have been recorded by most European countries, the US, Canada and Australia, but not Romania. The aim of this study is to analyze the prevalence and severity of FA and to assess the extent of information the medical and teaching staff in schools have on students' medical history.</p><p><strong>Methods: </strong>A cross-sectional survey was performed in schoolchildren from Cluj-Napoca, Romania, using an online questionnaire delivered to their parents.</p><p><strong>Results and conclusions: </strong>Seven hundred and eight individuals completed the entire questionnaire. The prevalence of self-reported FA was 8.9%, 28.6% presented food-induced angioedema and 38.1% required ER presentation. Cow milk (36.5%), egg (9.5%), strawberry (20.6%) and nuts (2.7%)were the most frequent culprit foods. The lack of an appropriate and accurate communication with the medical and teaching staff in the school suggest the requirement for further measures for parents and children educations regarding food allergy detection and management.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"5 ","pages":"1472673"},"PeriodicalIF":3.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}