International Archives of Allergy and Immunology最新文献

Introduction: Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants with widespread human exposure and have been associated with adverse health outcomes. However, their potential relationship with psoriasis remains insufficiently explored. The aim of this study was to investigate the association between PAH exposure and psoriasis.

Methods: Data were obtained from the National Health and Nutrition Examination Survey (NHANES) for the periods 2005-2006, 2009-2010, and 2011-2012. Weighted multivariate logistic regression analysis was performed to assess the association between individual PAH metabolites and psoriasis. Bayesian kernel machine regression, quantile g-computation (qgcomp), and weighted quantile sum regression were used to evaluate the relationship between mixed PAH exposure and psoriasis, as well as to determine the relative contributions of specific PAH metabolites. Stratified and sensitivity analyses were conducted to assess result stability.

Results: A total of 4,912 participants (mean age, 43.52 years; 95% confidence interval, 42.65-44.39 years) were included, of whom 2,514 (51.18%) were female, and 141 (2.87%) were diagnosed with psoriasis. Multivariate logistic regression analysis identified significant positive associations between psoriasis and seven urinary PAH metabolites: 2-hydroxynaphthalene, 3-hydroxyfluorene, 2-hydroxyfluorene, 3-hydroxyphenanthrene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, and 1-hydroxypyrene. Analysis of mixed exposure PAH across all three models demonstrated significant positive associations between urinary PAH metabolites and psoriasis, with 2-hydroxyphenanthrene and 2-hydroxynaphthalene identified as primary contributors. Stratified and sensitivity analyses confirmed the robustness of these results, and the observed associations persisted among nonsmokers.

Conclusion: Both single and mixed exposure analyses demonstrated a positive association between PAH exposure and psoriasis. These findings suggest that reducing PAH exposure may help mitigate psoriasis risk.

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.

Introduction: Allergic sensitization varies by region and environmental conditions. Given Peru's diverse climatic conditions, this study aimed to assess the relationship between climate variability and IgE-mediated sensitization patterns in four Peruvian cities.

Methods: Patients aged 3 to 70 years diagnosed with allergic rhinitis and/or asthma were recruited in Piura, Lima, Tarapoto, and Arequipa. Cities were classified using the Thornthwaite methodology adopted by SENAMHI. IgE-mediated sensitization was evaluated through skin prick tests and the Allergy Explorer 2 assay to detect reactivity to molecular allergen components. Chi-square analysis and Tukey's multiple comparisons identified significant differences among climatic zones.

Results: Allergic sensitization patterns varied across climate regions. In temperate arid zones, Blo t 5 sensitization was higher (25.3%) compared to warm arid zones (6.3%, p = 0.050). Fel d 1 sensitization showed marked regional differences (56.0% in temperate arid vs. 18.4% in warm rainy zones, p = 0.003). Despite having the highest humidity (92.3%), Tarapoto showed lower sensitization rates across all molecular components for mites in comparison with cities that are also characterized by high humidity, with most differences reaching statistical significance (p < 0.001). Pet allergen sensitization demonstrated climate-dependent variations, with both Fel d 1 and Can f 1 showing higher rates in temperate arid zones.

Conclusion: Peru's climatic diversity could be associated with distinct allergic IgE-mediated sensitization patterns, highlighting environmental factors' relevance in allergic disease management. Lower mite sensitization in the highest humidity zone suggests factors beyond humidity influence regional allergen sensitization patterns.

Introduction: Chronic rhinosinusitis with nasal polyps has a high post-surgery recurrence, suggesting complex pathology. However, research into underlying mechanisms and contributing factors, such as gut microbiota, is lacking. This study aimed to investigate the causal relationship between nasal polyps and gut microbiota, and to identify and quantify the potential mediating roles of metabolic pathways. We investigated the cause-and-effect relationship between nasal polyps and the gut microbiota and determined the influence of metabolic pathways as possible mediators.

Methods: This study utilized genetic data from genome-wide association studies. The datasets included nasal polyp data from FinnGen (6,841 cases and 308,457 control samples), microbial metabolic pathway data from the Dutch Microbiome Project (7,738 samples), and single-nucleotide polymorphisms of the gut microbiota from MiBioGen (18,340 samples). First, two-sample Mendelian randomization (MR) analyses were conducted on the gut microbiota, nasal polyps, and metabolic pathways. Next, a two-step MR was employed for mediation analysis to investigate whether metabolic pathways serve as mediators between the gut microbiota and nasal polyps and to estimate the proportion of the effect of metabolism-mediated gut microbiota on nasal polyps.

Results: MR analysis revealed that genus Actinomyces and genus Bifidobacterium are associated with an increased risk of nasal polyps through the inhibition of SO4ASSIM-PWY: sulfate reduction I (assimilatory) and PWY-4242: pantothenate and coenzyme A biosynthesis III, respectively. In contrast, family Desulfovibrionaceae is linked to a reduced risk of nasal polyps by promoting GALACTUROCAT-PWY: d-galacturonate degradation I. Additionally, the order Desulfovibrionales further mitigates the risk of nasal polyps not only by promoting the same GALACTUROCAT-PWY pathway but also by enhancing the ILEUSYN-PWY pathway, which involves l-isoleucine biosynthesis I derived from threonine.

Conclusion: This study identified a causal relationship between the gut microbiota and nasal polyps, with metabolic pathways as mediators. Our study provides new perspectives and possibilities for the study and treatment of chronic rhinosinusitis with nasal polyps.

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.