International Archives of Allergy and Immunology最新文献

Introduction: The global burden of respiratory allergic diseases linked to outdoor allergens remains poorly quantified despite increasing evidence of the allergens' impacts on respiratory allergic diseases. This systematic review synthesizes epidemiological evidence on the association between exposure to outdoor airborne allergens and respiratory disease incidence.

Methods: Following PRISMA 2020 guidelines, we systematically searched three databases, PubMed, Embase, and the Cochrane Library, until December 2024. Observational studies reporting effect estimates for respiratory outcomes (asthma, allergic rhinitis, COPD exacerbations, and cough) associated with quantified outdoor allergen exposure were eligible. Two reviewers independently conducted screening, data extraction, and quality assessment using an adapted Newcastle-Ottawa Scale (NOS). Random-effects models were employed to pool odds ratios (ORs), with subgroup analyses by sex. Publication bias was evaluated using Begg's and Egger's tests, respectively.

Results: From 6,551 identified records, 7 articles with 70 studies (46,325 participants across 3 countries) met the inclusion criteria. High-quality studies (NOS ≥7) constituted 86% of the included articles. Pooled analyses revealed significant associations between outdoor allergen exposure and respiratory outcomes: OR = 1.03 (95% confidence interval [CI]: 1.01-1.04; p = 0.008). Egger's publication bias was non-significant (Egger's p = 0.21), and Begg's publication bias was also non-significant (Begg's p = 0.31). Trim-and-fill funnel plots suggested possible missing small-null studies, but the statistical analysis was non-significant. Sensitivity analyses confirmed robustness when excluding studies with potential residual confounding (pooled OR range: 1.02-1.06). Subgroup analyses demonstrated that the female subgroup, rather than the male subgroup, got stronger effects significantly: OR = 1.04 (95% CI: 1.01-1.07), compared with the male subgroup OR = 1.02 (95% CI: 0.99-1.04).

Conclusions: This comprehensive synthesis provides high-quality evidence that outdoor allergen exposure significantly increases risks of respiratory allergic disease. The female is more likely to get respiratory morbidity compared with the male. Further research should prioritize harmonized exposure metrics and evaluate interactive effects with anthropogenic air pollutants.

Introduction: In the sub-Saharan area, data regarding total IgE levels particularly among apparently healthy population remain rare. Defining the IgE profile is crucial to identify allergic diseases driven by westernized lifestyles as elevated IgE may compromise safety of blood transfusion. The aim of the study was to assess total IgE levels in blood donors, investigate a possible correlation with sociodemographic, environmental, and biological parameters such as parasitic infestation and discuss their implications for public health and allergy in West Africa.

Methods: We carried out a prospective cross-sectional, descriptive and analytical study among blood donors. Information on the participants' allergy history as well as relevant environmental exposures were collected. Total IgE determination was performed by chemiluminescence, and stool samples underwent parasitological examination.

Results: More than 30% of the donors had elevated total IgE. Stool parasite examinations were positive in 18% of blood donors with 2% helminthiasis. There was a significant relationship between age (p = 0.00, correlation coefficient = -0.22), eosinophil count (p = 0.003, correlation coefficient = -0.60), and total IgE indicating that age and eosinophils counts are associated with increased total IgE concentrations. Highest median of total IgE levels was seen in parasitized people regardless of atopic status supported the idea that parasitic infection is an important factor of total IgE level.

Conclusion: Continuing assessments are important to understand these high levels of IgE in blood donors. Since elevated total IgE can also occur in non-allergic state, we need to integrate surveillance strategies that address both parasitic infections and allergic diseases completed by others relevant investigations for more comprehensive approach in West Africa.

Background: Allergic diseases represent a growing public health challenge due to aberrant immune responses to harmless environmental substances. Natural compounds have emerged as potential modulators of these responses. Cinnamon, a widely used spice with a rich profile of bioactive constituents, has demonstrated notable anti-inflammatory and immunomodulatory properties. This narrative review aimed to synthesize current in vitro and in vivo evidence regarding the effects of cinnamon and its derivatives on allergic disease mechanisms.

Summary: This narrative review compiles and critically examines findings from experimental studies that investigated the influence of cinnamon on key immunologic processes involved in allergic conditions. The review focuses on the modulation of antigen presentation by dendritic cells and macrophages, alterations in T-cell responses, mast cell stabilization, and the attenuation of airway and skin inflammation. Evidence from various experimental models was integrated to elucidate the molecular pathways affected by cinnamon. The reviewed studies indicate that cinnamon extract can reduce antigen-presenting cell maturation by decreasing co-stimulatory molecule expression and suppressing pro-inflammatory cytokine production. Additionally, cinnamon appears to stabilize mast cells by impairing receptor binding and disrupting calcium signaling, leading to a reduction in histamine release and other inflammatory mediators. Evidence further suggests that cinnamon modulates T-cell responses by promoting a regulatory immune cell profile and diminishing overall cytokine secretion. In experimental models of respiratory and skin allergies, treatment with cinnamon or its active compounds was associated with decreased inflammatory cell infiltration, improved airway function, and reduced severity of dermatitis-like lesions.

Key messages: The collective evidence from experimental studies suggests that cinnamon holds promise as a natural, multi-target therapeutic agent in managing allergic diseases. Its ability to modulate antigen presentation, stabilize mast cells, and promote regulatory immune responses supports its potential use as an adjunctive treatment for conditions such as asthma, allergic rhinitis, and atopic dermatitis. Further clinical investigations are warranted to optimize dosing strategies, formulations, and long-term safety for its practical application in allergic disease management.

Introduction: Sesame allergy is reported to be a major trigger of food-induced anaphylaxis and is associated with increased risk of accidental exposure. This study aimed to assess the efficacy and safety of a modified sesame desensitization protocol in children in real-world clinical practice.

Methods: Children with a positive skin prick test and a history consistent with an IgE-mediated allergy to sesame presenting at the Allergy Clinic of the Montreal Children's Hospital were recruited. After parents provided informed consent, an initial dose of sesame protein was introduced in the form of baked sesame paste (tahini) muffin or raw sesame seeds under physician supervision. An initial dose of 1/4 teaspoon (5 mg sesame protein) was given to the baked group, reaching a maintenance dose of two teaspoons of hummus (600 mg protein). In contrast, 75 mg of crushed sesame seeds (approximately 15 seeds) was given to the seeds group, reaching a maintenance dose of one tablespoon (3 g protein) of tahini. Once a maintenance dose was achieved, participants were asked to return to the clinic once a year for 5 years.

Results: The cohort consisted of 76 patients, in which 39 received baked sesame and 37 raw sesame. Considering the two desensitization strategies, using seeds significantly increased the odds of being at a higher reaction severity level by a factor of 7.1 (95% CI: 3.6-14.1) than baked goods with sesame paste. For both the baked goods and the seeds group, likelihood of severe reactions significantly decreased over time.

Conclusion: A modified sesame desensitization protocol using baked sesame paste can be safely used for children with sesame allergy.

Introduction: This study analyzed the value of serum amyloid A (SAA), interleukin-17 (IL-17), and the T helper cell 17/regulatory T cell (Th17/Treg) ratio in the clinical diagnosis and prognostic evaluation of lower respiratory tract infection (LRTI) in elderly patients with chronic obstructive pulmonary disease (COPD).

Methods: A retrospective analysis was performed on 214 elderly COPD patients hospitalized between January 2022 and December 2023. Patients were divided into infection (n = 101) and non-infection groups (n = 113) based on microbiological findings. Serum SAA, IL-17 levels, and peripheral Th17/Treg ratios at admission were measured and correlated with pulmonary function indices (forced expiratory volume in 1 s [FEV1], forced vital capacity [FVC], FEV1/FVC).

Results: In the infection group, SAA, IL-17 levels, and Th17/Treg ratio were higher (p < 0.05), while pulmonary function indices were lower (p < 0.05) than in the non-infection group. Receiver operating characteristic curve analysis showed combined detection of SAA, IL-17, and Th17/Treg had a higher diagnostic value (AUC = 0.970) than single indicators. Within the infection group, patients were further stratified by 60-day outcomes into favorable and poor prognosis subgroups. Multivariate logistic regression identified prolonged glucocorticoid therapy, elevated SAA, and increased Th17/Treg ratio as independent risk factors for poor prognosis, whereas IL-17 and mechanical ventilation were not statistically associated (p > 0.05). Combined biomarker analysis also yielded a strong prognostic performance (AUC = 0.874).

Conclusion: The combined assessment of SAA, IL-17, and Th17/Treg holds considerable value in the diagnosis and prognostic evaluation of LRTI in elderly COPD patients, providing new diagnostic and prognostic assessment tools for clinical practice.

Introduction: Genetic studies have investigated the association of genetic variants with immunoglobulin G4-related disease (IgG4-RD). In this study, we summarize the results of genetic association in IgG4-RD.

Materials and methods: We performed a literature search in MEDLINE, EMBASE via the OVID platform, Cochrane Central Register of Controlled Trials (CENTRAL), ClinicalTrials.gov (www.

Clinicaltrials: gov), and World Health Organization International Clinical Trials Registry Platform (WHO ICTRP) for genetic studies on IgG4-RD on January 20, 2023.

Results: We identified a total of 431 articles published between 1975 and 2023. After removing all the duplicates, we evaluated the abstract and selected 65 articles for full-text review. Among them, 17 fulfilled the eligibility criteria, including 15 original case-control studies, and two genome-wide association studies. Autoimmune pancreatitis was reported in 15 of the 17 articles, and the other 2 articles included IgG4-related periaortitis/periarteritis and general IgG4-RD subjects. A total of 52 polymorphisms in 25 genes were evaluated, including 13 polymorphisms in the 4 genes of the major histocompatibility complex (MHC) complex. The other genes are involved in different pathways.

Conclusion: While MHC associations remain the strongest and most consistent across studies, our review identifies emerging non-MHC genetic loci such as KCNA3, CTLA4, PRSS1, and VPS13B, suggesting distinct immune- and tissue-specific pathways in different IgG4-RD phenotypes.

Introduction: In recent years, coastal cities like Dalian have experienced a notable rise in pollen-induced allergic rhinitis (PiAR). This trend highlights the urgent need to investigate how climatic changes and air pollution exacerbate this growing public health challenge. This study examines the combined effects of meteorological variables, air pollutants, and airborne pollen on weed PiAR symptoms in Dalian, a coastal city located in the warm temperate zone of China.

Methods: Daily pollen concentrations were monitored from August to October 2023, concurrently with meteorological data and air quality indices. Clinical data, including symptoms and fractional exhaled nitric oxide (FENO) levels, were collected from 61 PiAR patients to evaluate the impact of environmental factors on allergy severity and airway inflammation.

Results: Among meteorological variables, temperature exhibited a positive influence on the concentrations of total pollen, specifically that of Artemisia, Humulus, and Chenopodium pollen, while air pressure showed an inverse relationship. Regarding air pollutants, O₃ concentration was positively associated with Artemisia pollen levels, whereas CO and NO₂ were negatively associated. Statistical analysis demonstrated a strong positive correlation between daily weed pollen concentrations and the Combined Symptom and Medication Score (CSMS) (r = 0.81, p < 0.0001), as well as between weekly average pollen concentrations and the Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) score (r = 0.95, p < 0.0001). Pollen exposure showed a significant immediate effect on CSMS at lag 0 (EE = 0.205, 95% CI: 0.076-0.334), while air pressure exhibited significant lagged and cumulative effects during lag days 0-5 (EE = 0.815, 95% CI: 0.337-1.293). Notably, the interaction between temperature and air pressure was also statistically significant (p < 0.001). Additionally, FENO levels in PiAR patients significantly rose during the peak weed pollen season (p < 0.001), indicating elevated airway inflammation.

Conclusion: This study highlights the complex interplay between meteorological factors, air pollutants, and pollen in exacerbating allergic symptoms. The findings underscore the need for integrated environmental and clinical management strategies to mitigate the burden of PiAR in urban settings.

Rheumatoid arthritis (RA) is a chronic debilitating autoimmune disorder and a predominant cause of potentially treatable functional disability. Adenosine deaminase acting on RNA 1 (ADAR1), as an RNA-editing enzyme, can regulate circular RNAs (circRNAs) and fibroblast-like synoviocytes (FLSs)-derived exosomal circFTO has been proposed as a contributor to RA. This study was dedicated to elaborate the role of ADAR1 in RA and the association between ADAR1 and circFTO. RT-qPCR examined circFTO, fat mass and obesity-associated protein (FTO), DExH-box helicase 9 (DHX9), ADAR1 and Quaking (QKI) expressions in RA-FLSs and human fibroblast-like synoviocytes (HFLSs), and circFTO expression in RA-FLSs- or HFLSs-derived exosomes. In severe combined immunodeficiency (SCID) mice engrafted with human cartilage and rheumatoid synovium tissue (SCID-HuRAg), the in vivo imaging technique was adopted to track the distribution and migration of RA-FLSs and HFLSs. H&E staining and Safranin-O staining measured the severity of RA and engrafted cartilage degradation. Immunohistochemistry assessed the expression of inflammation-, anabolic- and catabolic-related genes. Also, RT-qPCR examined the expressions of circFTO, miR-548a-3p, heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1), anabolic- and catabolic-related genes. ADAR1 was lowly expressed in RA-FLSs and ADAR1 silencing reduced circFTO expression in RA-FLSs-derived exosomes. In vivo, RA-FLSs were widely distributed and the migration capability was enhanced compared with HFLSs. ADAR1 overexpression efficiently decreased arthritis severity, attenuated cartilage degradation and inflammatory response in SCID-HuRAg mice injected with RA-FLSs. Besides, ADAR1 could decrease circFTO and hnRNPA2B1 expressions while elevating miR-548a-3p expression, particularly in SCID-HuRAg mice injected with RA-FLSs. To summarize, our findings identify ADAR1 as a potential treatment target for RA at least partially via regulating circFTO.

Background: Atopic dermatitis (AD) is a chronic inflammatory skin condition characterized by impaired barrier function, immune dysregulation, and severe pruritus. Recent studies have highlighted the pivotal role of neuronal regulation in modulating inflammation within the skin. Neuroimmune interactions, particularly between sensory neurons and immune cells, such as macrophages and mast cells, contribute significantly to the pathophysiology of AD. Additionally, neuropeptides and neurotrophins, including substance P and neurotrophin-4, have been implicated in amplifying inflammation and promoting skin barrier dysfunction.

Summary: This review explores the complex mechanisms underlying neuronal regulation of inflammation in AD, emphasizing the bidirectional communication between the nervous and immune systems. The review further emphasizes that pruritus is a primary driver of disease burden and should be a co-primary therapeutic target alongside inflammation control. The review also discusses emerging therapeutic strategies targeting neuroimmune circuits, including biologic agents against pruritogenic cytokines, kinase inhibitors, and neuropeptide antagonists. Finally, we address the role of adjunctive topical strategies, such as moisturizers containing topical anesthetics and calming botanical agents, which act to dampen neuronal excitability and support barrier repair.

Key messages: Collectively, these approaches offer novel and multifaceted strategies for managing both pruritus and inflammation in AD. Understanding these neuroimmune pathways is crucial for developing more effective, targeted treatments for this debilitating condition.

Background: Dendritic cells (DCs) represent a heterogeneous subpopulation of antigen-presenting cells that bridge the innate and acquired immune responses. Studies have reported that cellular metabolic reprogramming regulates the biological function of DCs, with distinct metabolic profiles characterizing different DC subsets and activation states. Particularly, blood monocyte-derived dendritic cells (mo-DCs) drive the skin inflammation. The differentiation, maturation, metabolism, and function of mo-DCs are influenced by microenvironmental factors, including pH, mechanical force, and temperature.

Summary: The paper briefly reviewed the biological role of mo-DCs in skin diseases, focusing on their differentiation and phenotype, disease-associated metabolic adaptations, and the microenvironmental factors that influence their maturation, energy metabolism, and function. Future researchers should explore the impact of the skin microenvironment on the metabolism and function of mo-DCs and identify specific targets, which may pave the way for precision medicine methods for treating refractory inflammatory skin diseases.

Key messages: With the understanding of mo-DC metabolism and its regulation by microenvironmental factors, we have gained further insight into the mechanism of skin diseases. However, we still need to discover the role of the skin microenvironment in mo-DC metabolism and function.