Frontiers in allergy最新文献

Background: A disintegrin and metalloproteinase 8 (ADAM8) has been implicated in eosinophilic inflammation; however, its role in chronic rhinosinusitis with nasal polyps (CRSwNP) remains to be elucidated. This study aimed to investigate the predictive significance of ADAM8 levels in nasal secretions for the endotypes and disease control status of CRSwNP.

Methods: A cohort comprising 120 CRSwNP patients and 45 healthy controls (HCs) was assembled, delineating 53 non-eosinophilic CRSwNP (neCRSwNP) and 67 eosinophilic CRSwNP (eCRSwNP) patients. Immunohistochemistry and enzyme-linked immunosorbent assay (ELISA) were utilized to measure ADAM8 levels in nasal mucosal tissues and secretions from all participants. The receiver operating characteristic (ROC) curves and Pearson correlation analysis were employed to assess the predictive capability of ADAM8 levels in predictiving CRSwNP endotypes and disease control status.

Results: ADAM8 levels in nasal secretions were elevated in CRSwNP patients compared to HCs, with a more pronounced increase observed in eCRSwNP patients. Elevated ADAM8 concentrations in nasal secretions were positively correlated with peripheral blood eosinophil counts and percentages, tissue eosinophil counts, serum total IgE, Lund-Mackay scores, and Lund-Kennedy scores. Ultimately, 103 CRSwNP patients completed the follow-up protocol, with 72 classified as the controlled group and 31 as the uncontrolled group. Uncontrolled CRSwNP patients exhibited significantly higher ADAM8 levels in nasal secretions compared to the controlled group. The ROC curves indicated that ADAM8 in nasal secretions exhibits robust discriminatory capacity for eCRSwNP and postoperative disease control status.

Conclusion: ADAM8 in nasal secretions emerges as a potential novel biomarker for the prognostication of CRSwNP endotypes and the postoperative disease control status.

Food allergy represents an increasing global health issue, significantly impacting society on a personal and on a systems-wide level. The gold standard for diagnosing food allergy, the oral food challenge, is time-consuming, expensive, and carries risks of allergic reactions, with unpredictable severity. There is, therefore, an urgent need for more accurate, scalable, predictive diagnostic techniques. In this review, we discuss possible future directions in the world of food allergy diagnosis. We start by describing the current clinical approach to food allergy diagnosis, highlighting novel diagnostic methods recommended for use in clinical practice, such as the basophil activation test and molecular allergology, and go on to discuss tests that require more research before they can be applied to routine clinical use, including the mast cell activation test and bead-based epitope assay. Finally, we consider exploratory approaches, such as IgE glycosylation, IgG4, T and B cell assays, microbiome analysis, and plasma cytokines. Artificial intelligence is assessed for potential integrated interpretation of panels of diagnostic tests. Overall, a framework is proposed suggesting how combining established and emerging technologies can effectively enhance the accuracy of food allergy diagnosis in the future.

Asthma has become one of the most serious chronic respiratory diseases threatening people's lives worldwide. The pathogenesis of asthma is complex and driven by numerous cells and their interactions, which contribute to its genetic and phenotypic heterogeneity. The clinical characteristic is insufficient for the precision of patient classification and therapies; thus, a combination of the functional or pathophysiological mechanism and clinical phenotype proposes a new concept called "asthma endophenotype" representing various patient subtypes defined by distinct pathophysiological mechanisms. High-throughput omics approaches including genomics, epigenomics, transcriptomics, proteomics, metabolomics and microbiome enable us to investigate the pathogenetic heterogeneity of diverse endophenotypes and the underlying mechanisms from different angles. In this review, we provide a comprehensive overview of the roles of diverse cell types in the pathophysiology and heterogeneity of asthma and present a current perspective on their contribution into the bidirectional interaction between airway inflammation and airway remodeling. We next discussed how integrated analysis of multi-omics data via machine learning can systematically characterize the molecular and biological profiles of genetic heterogeneity of asthma phenotype. The current application of multi-omics approaches on patient stratification and therapies will be described. Integrating multi-omics and clinical data will provide more insights into the key pathogenic mechanism in asthma heterogeneity and reshape the strategies for asthma management and treatment.

Context: Recent insights into type 2 inflammation have led to the development of monoclonal antibody therapies for severe asthma and chronic rhinosinusitis with nasal polyps (CRSwNP). Despite add-on therapy with a monoclonal antibody, some individuals remain uncontrolled in terms of upper and/or lower airway symptoms, prompting an exploration of the efficacy of combining biological therapies and their impact on inflammatory pathways.

Objectives: In this article, we present a distinctive case of a patient with CRSwNP, severe eosinophilic asthma, and uncontrolled upper airway symptoms, who experienced substantial clinical and local inflammatory improvements through dual monoclonal antibody therapy.

Methods: We provide a detailed case description and analysis of the patient's nasal tissue and secretions to gain insights into the local nasal inflammation under this unique therapeutic approach.

Results: The addition of an anti-IL-4Rα antibody led to an improvement in upper airway symptoms and a reduction in both eosinophilic and neutrophilic inflammation, despite prior anti-IL-5 therapy. These effects were consistently observed in both polyp tissue and nasal secretions.

Conclusion: Our patient, with CRSwNP, severe eosinophilic asthma, and uncontrolled upper airway symptoms, experienced substantial improvement with dual monoclonal antibody therapy, without major complications or side effects.

The Acari Hypothesis posits that acarians, i.e., mites and ticks, are operative agents of allergy. It derived from observations that allergens are molecular elements of acarians or acarian foodstuffs. A corollary of The Hypothesis provides how acarian dietary elements are selected as allergens; namely, a pattern recognition receptor native to the acarian digestive tract complexes with dietary molecules problematic to the acarian. By virtue of its interspecies operability, the receptor then enables not only removal of the dietary elements by the acarian immune system, but also-should such a complex be inoculated into a human-production of an element-specific IgE. Because pattern recognition receptors bind to molecules problematic to the organism from which the receptors originate, it follows that molecules targeted by adaptive IgE, i.e., allergens, must be problematic to acarians. This claim is supported by evidence that host organisms, when infested by acarians, upregulate representative members of allergenic molecular families. Appreciation of the relationship between allergens and acarians provides insight well beyond allergy, shedding light also on the anti-acarian defenses of many living things, especially humans.

This case describes a patient with anaphylaxis caused by traditional Chinese medicine. Skin prick test with the traditional Chinese medicine decoction indicates that he was allergic to Suan Zao Ren. The patient had pollinosis and had never taken Suan Zao Ren before, thus we need to think the possibility of pollen food allergy syndrome. This paper also proposes a procedure for doctors to identify the specific culprit of traditional Chinese medicine decoction.

Introduction: Asthma, a global chronic respiratory condition, varies in patient autonomy due to limited resources, health literacy, and cultural beliefs, emphasizing the importance of understanding this autonomy for improved asthma management.

Methods: A cross-sectional study was conducted at Jimma University Comprehensive Specialized Hospital, involving face-to-face interviews with 175 patients. Data was collected on sociodemographic characteristics, clinical factors, and autonomy levels using a validated Patient Autonomy Preference Index. Descriptive statistics and binary logistic regression analysis were used.

Results: A total of 175 participants were recruited, out of them 41.7% (95% CI: 31.19, 40.41)) of participants were autonomous in managing their asthma exacerbation. 127 (72.6%) of study participants were female, with a mean age of 47.51 (SD ± 13.96), 101(57.7%) were live in urban areas, 54 (30.9%) had no formal education, 140 (80%) were married, 112 (64%) had health insurance, and 102(83.3%) obtained health information about their condition from healthcare workers. Reside in an urban area (AOR = 3.24; 95% CI: 1.40-7.49, p < 0.006), have health insurance (AOR = 4.30; 95% CI: 1.76-10.51, p < 0.001), those doing regular exercise (AOR = 4.79; 95% CI: 1.69-13.64, p < 0.003), have family history (AOR = 7.47; 95% CI: 1.61-34.60, p < 0.01), have a duration above five years since diagnosis (AOR = 0.44; 95% CI: 1.04-1.26, p < 0.003), and participants with a high level of health literacy (AOR = 1.10; 95% CI: 1.00-1.20, p < 0.042) become associated with being autonomous in managing asthma exacerbation.

Conclusion and recommendation: Only around forty-two percent of study participants were autonomous in managing their asthma exacerbation. Thus healthcare providers should give due attention to those who reside in rural areas, are not insured, recently diagnosed with asthma, and with low health literacy to enhance patient autonomy and self-management practices, ultimately improving health outcomes for individuals with asthma.

Background: Long noncoding RNAs (lncRNAs) have been implicated in a diverse array of human immune diseases; however, a comprehensive understanding of the expression and function of lncRNAs in the peripheral blood leukocytes of individuals suffering from house dust mite (HDM)-induced allergic rhinitis (AR) remains elusive.

Objective: To explore the potential roles and functions of long noncoding RNAs (lncRNAs) in the pathogenesis of AR.

Methods: Sequencing analysis was performed on peripheral blood leukocytes collected from patients with HDM-induced AR and healthy controls (HCs) to elucidate the expression patterns of lncRNAs. Differentially expressed (DE) lncRNAs were identified and validated, and further correlation analyses were conducted to explore their associations with visual analog scale (VAS) scores and cytokine levels in the serum and nasal secretions. Additionally, bioinformatics analyses were performed to predict the potential pathways influenced by DE lncRNAs. Finally, the diagnostic potential of these lncRNAs in AR was assessed via receiver operating characteristic (ROC) curve analysis.

Results: Significant differences in the expression profiles of lncRNAs and mRNAs were detected between AR patients and HCs. Four lncRNAs were markedly upregulated in AR patients. AC011524.2 was positively correlated with nasal pruritus (r = 0.4492, P = 0.0411). AL133371.3 was positively correlated with runny nose (r = 0.4889, P = 0.0245). AC011524.2 was positively correlated with CXCL8 (r = 0.4504, P = 0.0035). AL133371.3 was significantly positively correlated with only IL-17 (r = 0.4028, P = 0.0100). IL-4 in the serum was positively related to IL-17 in the serum (r = 0.4163, P = 0.0002). CXCL5 in the serum was positively correlated with IFN-γ (r = 0.3336, P = 0.0354) in nasal secretions. The area under the curve (AUC) of the ROC curve resulting from the integration of the 4 lncRNAs exhibited a remarkable value of 0.940 for AR diagnosis.

Conclusions: Our results identified several lncRNAs associated with AR symptoms and inflammatory cytokines. Specifically, AC011524.2 and AL133371.3 exhibited strong correlations with diverse AR manifestations and serum cytokines, suggesting their pivotal role in the pathogenesis of AR, likely via neutrophil- and Th17-related pathways. However, the precise underlying mechanisms are still elusive, necessitating further exploration.

In addition to numerous clinical studies, research using experimental models have contributed extensive evidence to the link between antibiotic exposure and atopic disease. A number of mouse models of allergy have been developed and used to uncover the specific effects of various microbiota members and perturbations on allergy development. Studies in mice that lack microbes entirely have also demonstrated the various components of the immune system that require microbial exposure. The importance of the early-life period and the mechanisms by which atopy "protective" species identified in human cohorts promote immune development have been elucidated in mice. Finally, non-animal models involving human-derived cells shed light on specific effects of bacteria on human epithelial and immune responses. When considered alongside clinical cohort studies, experimental model systems have provided crucial evidence for the link between the neonatal gut microbiota and allergic disease, immensely supporting the stewardship of antibiotic administration in infants. The following review aims to describe the range of experimental models used for studying factors that affect the relationship between the gut microbiota and allergic disease and summarize key findings that have come from research in animal and in vitro models.