International Archives of Allergy and Immunology最新文献

Introduction: Tests for dog and cat allergen molecules might be useful to characterize individuals with clinical symptoms in unselected population samples. The aim of this study was to present prevalence data and to investigate airway symptoms to cats and dogs in relation to sensitization to cat and dog allergen molecules.

Methods: In a random sample from a population-based cohort aged 19 years, 595 subjects were tested for sensitization to airborne allergens. Sera from subjects with IgE levels > 0.10 kU/L to cat, dog or horse were further analyzed by microarray (ImmunoCAP™ISAC 112) for dog molecules Can f 1-6 and cat molecules Fel d 1, 2 and 4. Fel d 7 was analyzed with ImmunoCAP™. Information about symptoms of asthma and rhinoconjunctivitis upon cat and dog exposure was obtained by a structured interview.

Results: The most prevalent (51.6%) sensitizing dog allergen molecule was Can f 5. The prevalence of asthma upon dog contact increased from 0.9% in individuals negative to all tested dog molecules to 40% in individuals sensitized to six dog molecules. The prevalence of asthma upon dog contact was related to the number of dog lipocalin sensitizations independent of sensitization to Can f 5, whereas for rhinoconjunctivitis Can f 5 co-sensitization played a role. The most prevalent (91.2%) sensitizing cat molecule was Fel d 1 and co-sensitization to up to three molecules increased the prevalence of asthma when exposed to cat.

Conclusion: In individuals sensitized to cat as in individuals sensitized to dog, the prevalence of allergic symptoms increased with number of sensitizing allergen molecules. Individuals sensitized to dog had more complex sensitization patterns to allergen molecules compared to those sensitized to cat. Asthma upon dog exposure was mostly associated with dog lipocalin sensitization whereas Can f 5 sensitization increased the risk of rhinoconjunctivitis.

Background: Hereditary angioedema due to C1 inhibitor deficiency (HAE-C1INH) has a substantial impact on patients' health-related quality of life (HRQoL). While generic instruments are frequently used for assessment, they may not fully capture the disease-specific burden. This study aimed to evaluate HRQoL in patients with HAE-C1INH types I and II using validated, angioedema-specific tools.

Objective: To assess HRQoL and disease control in patients with HAE-C1INH and to investigate the association between attack localization and domain-specific quality of life impairments.

Methods: In this multicenter cross-sectional study, 82 patients with HAE-C1INH from six referral centers completed the Angioedema Control Test (AECT), Angioedema Activity Score (AAS-28), and Angioedema Quality of Life Questionnaire (AE-QoL). Family screening was conducted among those who consented.

Results: Patients experiencing attacks in the extremities (p<0.001) and laryngeal/pharyngeal regions (p=0.028) had significantly lower AECT scores, indicating poorer disease control. Higher AAS-28 scores were associated with attacks in the extremities (p=0.008), abdomen (p=0.018), face/neck (p=0.004), larynx/pharynx (p<0.001), and tongue/uvula/palate (p<0.001). AE-QoL scores revealed impaired quality of life across all attack locations. Subdomain analysis showed that abdominal attacks significantly impacted the Functioning (p=0.005) and Food (p=0.037) domains. Attacks involving the face/neck and larynx/pharynx were associated with substantial impairment in Fatigue/Mood (p=0.002, p=0.003), Functioning (p=0.044, p=0.002), and Fears/Shame (p=0.039, p=0.005) subdomains.

Conclusion: Attack localization in HAE-C1INH significantly influences disease control and HRQoL. Beyond assessing attack frequency, the use of disease-specific QoL tools allows for the identification of domain-specific impairments. Personalized treatment strategies targeting both symptom control and quality-of-life domains are essential for alleviating the long-term burden on patients and their families.

Background: Benralizumab, an anti-IL-5 receptor monoclonal antibody, induces near-complete eosinophil depletion and has demonstrated significant clinical benefits in severe eosinophilic asthma (SEA). Real-world data remain essential for evaluating its effectiveness outside controlled trial settings.

Objectives: To assess the clinical, laboratory, and functional outcomes of benralizumab over 32 weeks in a real-life cohort of SEA patients in Türkiye, following its recent national approval.

Methods: This retrospective study included biologic-naïve adults with SEA who initiated benralizumab between November 2023 and February 2025 and completed at least six consecutive doses. Peripheral blood eosinophil count (PBEC), clinically significant exacerbations (CSE), Asthma Control Test (ACT) scores, and spirometric parameters were evaluated at baseline and week 32. Patients were classified as responders (ACT ≥20 and no CSE) or non-responders.

Results: Twenty-four patients (66.7% female; mean age 50.9 ± 13.1 years) were included. Median PBEC decreased from 800 (230-2200) to 0 (0-100) cells/µL (p < 0.001). Median annual CSE frequency declined by 67% (p < 0.001). ACT scores improved from 9 (5-24) to 22 (9-25) (p < 0.001). Mean Forced expiratory volume in one second (FEV₁) increased from 1719 ± 768 mL to 2165 ± 831 mL (p < 0.001), while Forced vital capacity (FVC) showed significant improvement. Forced Expiratory Flow between 25% and 75% of the Forced Vital Capacity (FEF 25-75) exhibited a nonsignificant trend toward increase. Sixteen patients (66.7%) were classified as responders. Responders had higher baseline PBEC, FEV₁, and FEF25-75 values. Benralizumab was well tolerated, with only two mild adverse events observed.

Conclusion: Benralizumab provided substantial improvements in eosinophilic inflammation, exacerbation frequency, symptom control, and lung function over 32 weeks in a real-life SEA cohort. These findings support benralizumab as an effective and well-tolerated therapeutic option in routine clinical practice.

Introduction: This study was conducted to investigate how changes in self-perception in adolescents with chronic atopic diseases develop over time; and the influences of parenting, peer interactions, and school adaptation on these changes.

Methods: Data from the Korean Children & Youth Panel Survey (2010-2016) were analyzed, including 874 individuals with atopic diseases. Latent growth modeling was applied to analyze the changing pattern of self-perception and the factors affecting it.

Results: The self-perception scores indicated a tendency to increase as time passed. High levels of positive and low levels of negative parenting styles, as well as strong school adaption and peer attachment, impacted the high self-perception scores of adolescents who suffered from chronic conditions at various points in time over the longitudinal school ages.

Conclusion: The study highlights the importance of positive parenting, peer relationships, and school adaptation for youth with chronic atopic conditions. Efforts to improve these areas should continue.

Introduction: Allergen avoidance, the most effective strategy against allergic diseases, does not readily apply to indoor inhalant allergens. Capturing and eliminating allergens in the air could be an effective strategy. In this study, we tested the capability of titanium dioxide (TiO₂) to degrade allergens upon activation by a photocatalyst. House dust mite (HDM), cat, and oak pollen extracts were incubated with TiO₂ powder for 24 h in either dark or light exposure.

Methods: Changes in protein and allergen content (Der f 1, Fel d 1, and Que ac 1) were investigated by the Bradford assay and a 2-site ELISA. Protein profiles and IgE-reactive components were examined by SDS-PAGE and IgE immunoblotting. Inhibition ELISA was performed to evaluate allergenicity.

Results: Regarding protein concentrations, 69.9% of HDM, 27.1% of cat, and 21.5% of oak pollen proteins were degraded by TiO₂ compared to the allergen extracts incubated in the dark without TiO₂. More specifically, 96.6% of Der f 1 and 81.2% of Fel d 1 were degraded by investigatory rutile TiO₂, as measured by ELISA. However, no significant degradation of Que ac 1 was observed. Immunoblot analyses using mouse monoclonal antibodies against each allergen and IgE antibodies from patients' sera showed diminished allergen bands. In the inhibition ELISA of HDM extract containing various proteases, 87.1% and 96.5% of IgE reactivity was reduced by TiO₂, whereas 47.0% of self-degradation was observed.

Conclusion: TiO₂ eliminated each allergen molecule at a different degradation rate. TiO₂ may be useful in reducing indoor allergenic molecules. However, more detailed studies are needed to optimize its efficacy.

Introduction: Biological agents are essential treatment options for severe asthma, particularly in cases with type 2 (T2) inflammation, due to their ability to improve symptoms, prevent exacerbations, and reduce the use of oral corticosteroids. However, limited data exist regarding their long-term effects on lung function, particularly on forced expiratory volume in 1 s (FEV₁). This study aimed to analyze the longitudinal changes in FEV₁ before and after the initiation of biological agents by following cases over an extended period.

Methods: This study included patients with at least three spirometric measurements before and after the initiation of biological agents, and a follow-up period of at least 2 years. The primary outcome was the annual change in FEV₁ (ΔFEV₁). Secondary outcomes included comparisons between patients with improved and deteriorated ΔFEV₁, differences based on the type of biological agent used, and comparisons between patients who achieved clinical remission and those who did not.

Results: A total of 41 patients with severe asthma were analyzed. The overall ΔFEV₁ significantly improved after the introduction of biological agents (p < 0.001). Patients with greater declines in FEV₁ prior to treatment showed more pronounced improvements, especially among those treated with anti-IL-5 biologics (mepolizumab and benralizumab) or anti-IL-4 receptor antibodies (p = 0.016 and p = 0.026, respectively). Furthermore, patients with elevated T2 inflammation biomarkers, such as fractional exhaled nitric oxide and peripheral blood eosinophil count, exhibited greater improvements in FEV₁.

Conclusion: This study indicates that biological agents may help prevent the progressive decline in lung function in severe asthma, particularly among patients with significantly declined lung function or elevated T2 inflammation biomarkers before treatment. Further research is needed to explore differences in efficacy across various biological agents.

Introduction: Chronic urticaria (CU) negatively impacts children's quality of life (QoL), yet data on pediatric CU remain limited. This study assessed CU's impact on QoL using the Children's Dermatology Life Quality Index (CDLQI).

Methods: Children (4-16 years) with CU were recruited and completed standardized questionnaires on demographics, CU type, management, and comorbidities. Chart review assessed laboratory data. Patients also completed the Urticaria Control Test (UCT), Urticaria Activity Score over 7 days (UAS7), and CDLQI at study entry. Multivariable logistic regression identified factors associated with clinically poor QoL.

Results: Seventy-four children (median age = 10) were recruited: 39 (52.7%) had chronic spontaneous urticaria, 21 (27.0%) had chronic inducible urticaria, and 14 (16.2%) had both. Most children (n = 54; 72.9%) reported a clinically satisfactory (CDLQI ≤5), while 20 (27.0%) reported a clinically poor QoL (CDLQI >5). Factors associated with clinically poor QoL included older age at symptom onset (aOR = 1.04; 95% CI = 1.01-1.05), elevated C-reactive protein (CRP >5 mg/L) (aOR = 1.49; 95% CI = 1.04-2.13), and history of atopic dermatitis (aOR = 1.59; 95% CI = 1.18-2.13). In younger children (aged 4-10), cold urticaria was associated with clinically poor QoL (aOR = 1.44; 95% CI = 1.07, 2.00).

Conclusion: Older age at symptom onset, elevated CRP, atopic dermatitis, and cold urticaria are associated with clinically poor QoL in children with CU. These findings highlight the need for targeted interventions, such as psychosocial support and education, to improve patient outcomes.

Introduction: This study employs bibliometric methods to reveal research trends, hot topics, and development trajectories in the field of cow milk protein allergy (CMPA) in children.

Methods: We retrieved and downloaded literature on CMPA in children from the Web of Science Core Collection database on the basis of specific search strategies and screening criteria. Using VOSviewer software, we analyzed the collaboration networks among countries, institutions, and authors, as well as the co-occurrence of keywords. We utilized Biblioshiny software to analyze highly cited papers and research trend topics and to construct thematic maps.

Results: We included 1,128 articles related to pediatric CMPA for analysis. The results show that since 2014, the number of research papers on CMPA has increased. The USA, Italy, and China are the countries with the greatest number of publications, with the USA occupying a central position in the collaboration network. The Icahn School of Medicine at Mount Sinai ranks first in terms of research output. Professor Hugh A. Sampson is the most influential author in this field. The main research areas include clinical manifestations, molecular mechanisms, immune regulation, and immunotherapy for CMPA. Emerging research hotspots in recent years include the gut microbiome, the development of dairy substitutes, and the application of sandwich enzyme-linked immunosorbent assay (sELISA) technology in milk protein detection.

Conclusion: Through bibliometric analysis, this study revealed the research trends and hotspots in the field of CMPA in children. Future research should further strengthen international cooperation to promote in-depth research and effective management of CMPA.

In the article "Silencing of FSTL1 Alleviated LPS-Induced Inflammatory Damage and Oxidative Damage in Human Bronchial Epithelial Cells via BMP4/KLF4 Axis" [Int Arch Allergy Immunol. 2022;183(7):785-795. https://doi.org/10.1159/000521852] by Yi Zhang, Liping Yan, Jiao Yang and Xiangni Li, after publication, the authors identified an error in Figure 5a of their article.Fig. 5.Silencing FSTL1 promoted BMP4 and KLF4 expression. a Co-IP was used to study whether FSTL1 interacts directly with KLF4. b The expression levels of KLF4 and BMP4 were detected by Western blotting. c Quantitative value of BMP4 expression level. d Quantitative value of KLF4 expression level. ##p < 0.01 versus LPS + si-NC group. $p < 0.05 versus LPS + si-FSTL1 group. Co-IP, co-immunoprecipitation.Figure 5a was erroneously submitted by the authors as a draft sketch. The correct complete Figure 5 is shown here.The original article has been updated to reflect this.

Introduction: Asthma demonstrates a strong sex bias. B cells play critical roles in the pathogenesis of allergic inflammation, including allergen-specific immunoglobulin production. The sex-specific responses of B cell subsets in allergic lung inflammation remain unknown. This project aimed to study the sex differences in allergen-induced B cell subsets in a murine model of asthma.

Methods: Adult mice of both sexes were sensitized using two intraperitoneal injections of ovalbumin (OVA) on days 0 and 7. Mice were then challenged with intranasal OVA on days 14, 16, and 18 and euthanized 24 h after the last challenge. We examined whole-lung B-cell subsets using flow cytometry and whole-lung cytokine levels using ELISA or multiplex assay.

Results: OVA-treated female mice had significantly higher numbers of whole-lung naïve B cells and plasmablasts versus OVA-treated male mice. The numbers of IgM+ memory B cells and isotype-switched IgM- memory B cells in the lung trended higher in OVA-treated female mice. The lungs of OVA-treated female mice had increased C-C motif chemokine ligand 5, granulocyte-colony stimulating factor, IL-1β, and tumor necrosis factor-α protein levels, chemokines/cytokines involved in B-cell regulation, versus lungs from OVA-treated male mice. However, whole-lung B cell activating factor and a proliferation-inducing ligand levels showed no differences between male and female mice.

Conclusions: In a murine asthma model, sex differences in whole-lung B lymphocytes are primarily driven by higher numbers of naïve B cells and plasmablasts in females versus males. Our results suggest that sex chromosomes and sex hormones may influence B-cell subsets during allergic lung inflammation.