International Archives of Allergy and Immunology最新文献

Background: Airway cilia are essential for maintaining respiratory health by facilitating the removal of inhaled pathogens and toxicants through mucociliary clearance. However, daily exposure to environmental factors such as cigarette smoke, PM2.5, allergens, and microplastics can impair cilia structure and function, leading to compromised mucociliary clearance and the progression of respiratory diseases.

Summary: This review synthesizes recent research on the impact of common environmental exposures on airway cilia, focusing on structural and functional alterations, as well as associated signaling pathways. Emerging therapeutic strategies, including gene therapy, anti-inflammatory agents, and antioxidants, show promise in restoring ciliary function and improving mucociliary clearance.

Key messages: Environmental exposures impair airway cilia through multiple mechanisms, including oxidative stress, inflammation, and dysregulation of signaling pathways. Future research should focus on identifying novel therapeutic targets and developing personalized interventions to mitigate ciliary damage.

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: Ubiquitination and immune regulation play an important role in sepsis. The purpose of this study was to explore the potential value of ubiquitination- and immune-related genes in sepsis and develop a risk score prognostic model based on sepsis ubiquitination- and immune-related genes for accurate outcome prediction and better treatment guidance.

Methods: Differential expression and univariate Cox analyses were used to identify ubiquitination- and immune-related DEGs related to prognosis, and then a risk model was constructed using LASSO regression analysis. Subsequently, Kaplan-Meier analysis, time-dependent ROC curve analysis, immune cell infiltration analysis, functional enrichment analysis, drug prediction, and molecular docking were performed.

Results: A total of 4 ubiquitination- and immune-related DEGs related to the prognosis of sepsis were identified. A risk score model was constructed based on these 4 genes. The proportion of death samples in the high-risk score group was higher and the OS was worse. The risk score was an independent prognostic factor for sepsis. The time-dependent ROC curve indicated that the risk score model had good predictive ability. The results of ssGSEA and GSEA showed that most immune cell infiltration levels decreased and immune- and inflammation-related pathways showed inhibitory states in the high-risk group. In addition, 7 protein-drug docking results were obtained. The binding energy of LCK and JNJ-26483327 was the lowest.

Conclusion: The 4 ubiquitination- and immune-related model genes may play an important role in sepsis by regulating immune cell infiltration and immune- and inflammatory-related pathways. The model constructed based on these 4 genes has good predictive value, which may help clinical doctors better evaluate the prognosis of sepsis patients and develop personalized treatment plans.

Introduction: We aimed to assess the prevalence of IgE-mediated sensitization to two perennial (dust mite and animal) and four seasonal allergen sources (tree, grass, weed, and mold/fungi) using data from a national clinical reference laboratory (Quest Diagnostics).

Methods: Patients tested in 2019 for ≥1 specific serum IgE toward 4 dust mites, 14 animals, 32 trees, 12 grasses, 21 weeds, or 19 mold/fungi allergens were included. Patients with ≥1 specific IgE ≥0.10 kU/L within a source were considered sensitized for the source. Chi-square tests and multivariate logistic regression were used to compare the estimated prevalence of allergic sensitization related to demographics, geography, and clinical diagnosis.

Results: Sensitization for dust mite, animal, tree, grass, weed, and mold/fungi sources was 38.0% (21,161/55,735), 32.1% (21,888/68,035), 34.5% (22,975/66,567), 30.3% (21,664/71,575), 31.2% (22,960/73,605), and 19.7% (13,514/68,574), respectively. Across allergen sources, males had higher prevalence (from lowest to highest: 25.3% mold/fungi to 43.0% dust mite) compared to females (from lowest to highest: 16.1% mold/fungi to 34.6% dust mite); prevalence peaked in 10-19 years (from lowest to highest: 29.7% mold/fungi to 54.2% dust mite) and then decreased with increasing age; large metropolitan areas (from lowest to highest: 39.6% dust mite to 20.7% mold/fungi) had higher prevalence compared to small-to-medium metro (from lowest to highest: 36.6% dust mite to 17.9% mold/fungi) or nonmetro areas (from lowest to highest: 32.4% dust mite to 19.5% mold/fungi); a higher prevalence was observed in patients with asthma, atopic dermatitis, or rhinitis than in those with none of these diagnoses reported. Sensitization to perennial and seasonal allergens showed regional variation.

Conclusions: Prevalence of allergic sensitization to perennial and seasonal allergens is associated with patient age and sex, census regions, level of urbanization, and allergic disease states. These factors should be considered when designing and selecting allergen panels for diagnosing and treating symptomatic patients.

In the article "Concomitant Chronic Urticaria in Children: A Distinct Severe Phenotype" [Int Arch Allergy Immunol. 2025; https://doi.org/10.1159/000548050] by Alrafiaah et al., the first affiliation in the paper was wrongly given.The correct affiliation is given below.aDepartment of Pediatrics, College of Medicine, Majmaah University, Majmaah, Saudi Arabia.

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.

Introduction: Giant cell arteritis (GCA) is an autoimmune disease affecting medium and large arteries. It varies in presentation and often recurs, potentially leading to blindness and aneurysms. The pathogenesis of GCA is not well understood. This study aimed to identify key genes linked to GCA and explore potential pathogenic mechanisms.

Methods: This study integrated single-cell RNA sequencing, expression quantitative trait loci, and genome-wide association study data, employing a two-sample Mendelian randomization (MR) method to explore the causal effects of marker genes in CD4+ T cells on the development of GCA. Additionally, colocalization analysis was conducted to determine whether there was a shared causal variant.

Results: Through single-cell RNA sequencing and MR analysis, we identified three key genes, RCAN3, RPS6, and HLA-DQB1, that had a causal relationship with a reduced risk of GCA. Specifically, RCAN3 (OR = 0.49, 95% CI = 0.26-0.93, p = 0.03), RPS6 (OR = 0.21, 95% CI = 0.06-0.73, p = 0.01), and HLA-DQB1 (OR = 0.76, 95% CI = 0.62-0.93, p = 0.01) were inversely associated with the disease. Multiple sensitivity analysis methods showed no heterogeneity and pleiotropy, and ruled out potential reverse causality, demonstrating the robustness of MR analysis results. Colocalization analysis revealed that HLA-DQB1 and GCA were related to SNPs within the same genomic region but involved different causal variants.

Conclusions: This study identified three potential key genes (RCAN3, RPS6, and HLA-DQB1) linked to the causality of GCA, providing new perspectives on the pathogenesis of GCA and new avenues for therapeutic strategies.

Introduction: This study investigated the potential impact of maternal consumption of fermented products during pregnancy and lactation on the development of cow's milk protein allergy (CMPA) in infants. The introduction highlights how maternal diet can influence immune tolerance and the development of allergic diseases. Although the protective effects of fermented foods on various health conditions are recognized, evidence of their role in preventing allergic diseases remains inconclusive.

Methods: The research was conducted as a case-control study with 95 children aged 0-3 years, comprising 46 CMPA cases and 49 healthy controls. Data were collected through face-to-face interviews with mothers, focusing on demographic information, maternal diet, and environmental factors. Fermented product consumption was measured in grams and milliliters, and allergy diagnoses were confirmed via clinical evaluations, IgE tests, and oral food challenge tests.

Results: Our study analyzed 46 cases and 49 controls. Among cases, 67.4% (n = 31) had IgE-mediated CMPA, while 32.6% (n = 15) had non-IgE-mediated CMPA. Maternal smoking during pregnancy was reported in 4.3% of cases and 10.2% of controls (p = 0.437). Yogurt intake during pregnancy was lower in cases (230 g/week) than in controls (420 g/week) (p = 0.011), while cheese intake was 210 g/week and 225 g/week, respectively (p = 0.042).

Conclusion: The study concludes that maternal consumption of fermented products during pregnancy may reduce the risk of CMPA in infants. However, larger and long-term studies are needed to clarify the interaction between dietary, cultural, and environmental factors. Further investigation into variables like antacid use, probiotic supplementation, and infection history is also recommended to better understand their influence on CMPA development.